Indications include a decrease in systolic pressure of more than 30 mmHg from baseline or mean arterial pressure (MAP) less than 60 mmHg resulting in end-organ dysfunction. Common vasopressors are norepinephrine, epinephrine, phenylephrine, and vasopressin. medications that produce arteriole vasoconstriction via positive inotropic or chronotropic effects that lead to increased systemic vascular resistance and BP. (To view a detailed list of common vasopressors and inotropes, visit /?p=71893.) Vasopressors and inotropes are commonly used in the ICU to manage shock and support the cardiovascular system. Hypovolemia and decreased arterial blood volume stimulate vasopressin release via baroreceptors in the carotid sinuses and aortic arch, resulting in increased water retention that causes vascular smooth muscle constriction. Their stimulation results in vasoconstriction, primarily in the splanchnic, renal, and hepatic arteriole vasculature. V1 receptors are found in vascular smooth muscles. Arginine vasopressin, an antidiuretic hormone, is synthesized in the hypothalamus and controls the body’s osmotic balance, regulates BP, and influences water reabsorption in the kidneys. Dopamine receptor activation within the kidney vasculature leads to enhanced renal perfusion. As activation increases, vasoconstriction occurs via stimulation of a1 receptors and inhibition of norepinephrine release. Small doses of dopamine result in vasodilation. Site-specific dopamine receptors also exert cardiovascular actions. In addition, b2 receptors have a significant impact on smooth muscles in the airway and cause bronchodilation.ĭopamine receptors. Although b2 receptors cause vasodilation, their effect on cardiac output is less than that of b1. b2 receptors, which are located in the arterioles of the heart, smooth muscle tissues, and lungs, help mediate many essential processes. b1 receptor activation in the kidneys induces the release of renin into the blood, promoting angiotensin synthesis and elevating BP. Systemic vasodilation may offset increased cardiac output, resulting in decreased arterial pressures. It also increases heart rate and cardiac output. b1, the dominant receptor found in the heart and kidney, enhances myocardial contractility and relaxation when it’s activated. a2 receptors also are located on the nerve terminals of the peripheral nervous system and function to inhibit transmitter release.īeta receptors are found on the arterioles of the heart, smooth muscle tissues, and the lungs where they bind to circulating norepinephrine and epinephrine. When stimulated, they produce vasoconstriction. a1 receptors are located within the veins, arterioles, and many capillary beds. (See Receptor physiology.)Īdrenergic (alpha and beta), dopamine, and vasopressin receptors exert actions on specific organs.Īdrenergic receptors. Other receptors are vasopressin (V1 and V2 this article focuses on V1) and dopamine. Adrenergic receptors are classified as alpha (a1, a2) or beta (b1, b2), and their location determines their physiologic response. The parasympathetic system conserves and restores body processes during normal conditions, resulting in reduced heart rate, cardiac output, and BP.Īdrenergic receptors (which affect the sympathetic nervous system) within the heart and vascular system facilitate the hemodynamic effects of vasopressors via the interaction of catecholamines and synthetic medications such as norepinephrine and epinephrine. The sympathetic system prepares the body for stressful or emergent situations, resulting in increased heart rate and contractility, vasoconstriction, and norepinephrine and epinephrine release, which increase BP. Body processes activate the ANS in response to information produced by internal and external stimuli, including blood pressure, body temperature, heart rate, respiratory rate, metabolism, urination, defecation, digestion, and sexual response via chemical and neurotransmitter signaling. The ANS regulates the heart, secretory glands, and smooth muscles via activation of the parasympathetic and sympathetic systems. Short-term blood pressure (BP) regulation is controlled by the autonomic nervous system (ANS) via baroreceptors in the aortic arch and carotid sinus. Shock disrupts cardiovascular physiology, particularly blood pressure, so understanding normal function is important. When critical care nurses understand shock pathophysiology and hemodynamic monitoring, they can effectively and safely titrate (increase or decrease an infusion rate for therapeutic effect) these medications using the lowest possible dose to avoid adverse effects. Organ hypoperfusion results from decreased circulating volume (hypovolemic shock), decreased cardiac output (cardiogenic and obstructive), and vasodilation (distributive). Shock is a decline in tissue perfusion and oxygen delivery, leading to cellular dysfunction and death.
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