Running from a Bear: How We Teach Vasopressors, Adrenoreceptors, and Shock

Abstract

Vasopressors are widely used in the management of shock among critically ill patients. The physiology of vasopressors and adrenoreceptors and their effects on end organs therefore represent important, high-yield topics for learners in the critical care environment. In this report, we describe our approach to teaching this core concept using the stereotypical human physiologic response when running from a bear, in the context of the relevant supporting literature. We use escaping from a threatening predator as a lens to describe the end-organ effects of activating adrenoreceptors together with the effects of endogenous and exogenous catecholamines and vasopressors. After reviewing this foundational physiology, we transition to the clinical environment, reviewing the pathophysiology of various shock states. We then consolidate our teaching by integrating the physiology of adrenoreceptors with the pathophysiology of shock to understand the appropriateness of each therapy to various shock phenotypes. We emphasize to learners the importance of generating a hypothesis about a patient's physiology, testing that hypothesis with an intervention, and then revising the hypothesis as needed, a critical component in the management of critically ill patients.

Keywords: adrenoreceptors; clinical teaching; medical education; sepsis; shock.

Figure 1.

(A) End-organ effects of key adrenoreceptors. Agonism of key adrenoreceptors, including α-1, β-1, and β-2, leads to important effects on end organs that mediate the sympathetic response. As illustrated in the left panel, α-1 receptors dilate the pupils (enhancing vision) and mediate vasoconstriction of the splanchnic system and skin (to assist in shunting blood away from nonessential organs during a fight-or-flight response). β-1 receptors, depicted in the center panel, augment cardiac contractility and chronotropy, increasing stroke volume and heart rate, together resulting in enhanced cardiac output. β-2 receptors, shown in the right panel, lead to relaxation of smooth muscle. This results in bronchodilation (improving $\dot{\text{V}}$/$\dot{\text{Q}}$ matching and increased minute ventilation) as well as vasodilation of the vasculature in the smooth muscle, therefore achieving preferential shunting of blood to the muscles from nonessential organs. β-2 adrenoreceptor activation also leads to the release of lactate as a rapidly available energy source for the muscles and brain. (B) End-organ effects of key adrenoreceptors: easily reproducible illustration for whiteboard teaching. $\dot{\text{V}}$/$\dot{\text{Q}}$ = ventilation/perfusion.

Figure 2.

(A) Expected changes in hemodynamics during key shock states. Hypovolemic shock is mediated primarily by intravascular volume depletion. As a result, intracardiac pressures are decreased (i.e., central venous pressure [CVP], mean pulmonary arterial pressure [mPAP], and pulmonary capillary wedge pressure [PCWP]), as is cardiac output (CO), a result of decreased stroke volume. In contrast, systemic vascular resistance (SVR) increases to compensate before the delivery of adequate volume resuscitation. In cardiogenic shock, impaired CO leads to increases in the preceding circulatory pressure (i.e., PCWP, mPAP, and CVP) as well as a compensatory increase in SVR. The inappropriate systemic vasodilation of distributive shock leads to reduced SVR, CVP, and mPAP. CO can be variable and is often elevated with increases in heart rate and stroke volume. Finally, in obstructive shock, defined by an obstruction to forward flow, CO is diminished and preceding pressures are elevated (i.e., PCWP, mPAP, and CVP), as is SVR. (B) Expected changes in hemodynamics during key shock states: easily reproducible table for whiteboard teaching.