Introduction to CV Pharmacology - Orlando Health

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CV Pharmacology Vasopressor Therapy Clinical Application Vasopressor drugs must not be used until the patient’s volume status has been addressed. The administration of vasopressors to hypovolemic patients does not increase blood pressure; instead it can result in profound tachydysrhythmias and ventricular tachycardia or ventricular fibrillation. Should extravasation of this or any other alpha agonist occur, phentolamine (Regitine) may be used to help minimize tissue damage. Refer to your hospital’s policy regarding the use of phentolamine for intravenous extravasation of these drugs. Dopamine Dopamine (Intropin) is a chemical precursor of norepinephrine. Dopamine stimulates alpha, β 1 , and dopaminergic receptors, depending on the administered dose, and also stimulates the release of norepinephrine Indications Dopamine is used primarily for symptomatic hypotension and to increase organ perfusion. According to the ACLS bradycardia algorithm, dopamine may also be considered in hemodynamically significant bradycardia, with the dose beginning at 5 mcg/kg/minute, following the use of transcutaneous pacing and/or atropine. In patients with cardiogenic shock, left ventricular failure, and pulmonary edema, dopamine may be used in conjunction with positive inotropic agents and vasodilators. This permits the beneficial β 1 effects to predominate and counteracts the increases in preload and afterload caused by alpha stimulation. At low doses (1 – 4 mcg/kg/minute), dopamine stimulates the dopaminergic receptors to produce cerebral, renal, and mesenteric vasodilation. This dose is commonly thought to increase blood flow to the kidneys and may sometimes be referred to as the renal dose dopamine. The efficacy of dopamine for this indication is not supported in the literature. NOTE: Many clinicians currently suggest that low dose dopamine therapy does NOT prevent or ameliorate acute renal failure in patients. At moderate doses (5 -10 mcg/kg/minute), dopamine stimulates the β 1 receptors in the myocardium. This increases contractility, cardiac output, and arterial blood pressure. At higher doses (10 – 20 mcg/kg/minute), the alpha agonist properties of dopamine are much more pronounced, resulting in significant increases in peripheral and venous vasoconstriction. This results in an increase in preload, afterload, and myocardial workload. It also significantly increases myocardial oxygen demand and negates the positive β 1 and dopaminergic effects. At doses of 20 mcg/kg/minute or more, significant arterial vasoconstriction results. If hypotension continues, then other interventions should be considered. 2010 Orlando Health, Education & Development 35
CV Pharmacology Precautions and Interactions As with any of the vasopressors, the patient’s volume status should be addressed before the administration of dopamine. Failure to do so may result in tachydysrhythmias, ventricular tachycardia, and ventricular fibrillation. MAO inhibitors strongly potentiate dopamine so the dosage should be only 10% of the recommended dose. The arrhythmogenic potential of dopamine increases as the dose increases, as does the increase in myocardial workload and myocardial oxygen demand. Since low dose dopamine causes vasodilation of the mesenteric and renal vessels, it tends to shunt blood to the kidneys and intestines, and may actually result in a slight decrease in blood pressure. Clinical Application It is recommended that all dopamine doses be administered through a central venous catheter since extravasation of dopamine causes tissue necrosis. Epinephrine Epinephrine, also known as Adrenalin, is a naturally occurring catecholamine which stimulates both alpha and beta receptors.Epinephrine’s alpha agonist activity results in peripheral vasoconstriction, which increases systemic vascular resistance as well as systolic and diastolic blood pressure. This results in increased coronary and cerebral perfusion blood flow. Epinephrine’s beta-1 agonist activity increases automaticity and myocardial electrical activity, myocardial contractility and cardiac output. Its beta-2 agonist properties result in bronchodilation. Epinephrine also inhibits the release of histamine, which is responsible for the cardiovascular collapse that occurs in severe allergic reactions and anaphylaxis. Indications Epinephrine’s adrenergic agonist properties make it useful in any pulseless rhythm such as asystole, pulseless electrical activity, ventricular fibrillation, and pulseless ventricular tachycardia. It also facilitates these ventricular rhythms to be more responsive to defibrillation. Additionally, when used as a diluted continuous intravenous infusion, epinephrine is useful for profound symptomatic bradycardia that has not responded to a pacemaker or atropine. Epinephrine is also used in the management of anaphylactic shock. It relieves bronchospasm, causes bronchodilation, and blocks the release of histamine (histamine is the chemical mediator that leads to the vascular changes in anaphylaxis thus leading to shock). It is further recommended that epinephrine be administered through a central venous catheter since extravasation of epinephrine causes tissue necrosis. Precautions and Interactions Note: Medication errors have occurred due to confusion with epinephrine products expressed as ratio strengths (i.e. 1:1000 vs. 1:10,000). Epinephrine 1:1000 = 1 mg/mL and is most commonly used Sub Q for hypersensitivity reactions or as a bronchodilator. Epinephrine 1:10,000 = 0.1 mg/mL and is used I.V. as part of the ACLS protocol. © 2010 Orlando Health, Education & Development 36
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