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Vasopressors. Alpha Adrenergic Receptors. Activation of alpha-1 Postsynaptic adrenoreceptors located in smooth muscle throughout the body Increases intracellular calcium concentrations Blood vessels: Vasoconstriction Pancreas: Inhibits the release of insulin
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Alpha Adrenergic Receptors • Activation of alpha-1 • Postsynaptic adrenoreceptors located in smooth muscle throughout the body • Increases intracellular calcium concentrations • Blood vessels: Vasoconstriction • Pancreas: Inhibits the release of insulin • Intestine/Bladder: Relaxation, but constriction of sphincters • Activation of alpha-2 • Presynaptic receptors decreases NE release thru negative feedback • Brain receptors lowers the blood pressure (decreases SNS activity) and causes sedation
Beta Adrenergic Receptors • Beta-1 • Located primarily on post synaptic membranes of the heart • Positive chronotrope, dromotrope, and inotrope • Fat Cells: Lipolysis • Beta – 2 • Located primarily on post synaptic smooth muscle and gland cells • Blood Vessels: Vasodilation • Bronchioles: Bronchodilaton • Uterus: Relaxation of uterus • Kidneys: Renin Secretion • Liver: Gluconeogenesis, glycogenolysis • Pancreas: Insulin secretion
Dopaminergic Receptors • Dopamine-1 • Blood Vessels: Dilates renal, coronary, and splanchnic vessels • Dopamine-2 • Presynaptic endings: inhibits NE release • CNS: Psychic disturbances
Vasopressors • Phenylephrine • Primarily direct alpha-1 agonist with minimal beta affects • Arteriolar vasoconstriction • Dose 50-200mcg bolus • Duration 5 minutes • PROS: • increases CPP without increasing myocardial contractility (useful in CAD, hypertrophic subaortic stenosis, or aortic stenosis • CONS: • Decreased SV due to increased afterload, may increase PVR, may decrease perfusion to kidneys, gut and extremities
Vasopressors • Ephedrine • Mild direct alpha, beta -1 and beta-2 agonist • Primarily causes indirect release of NE • Dose 5-10mg IV bolus • Duration 3-10min • PROS: • Easy to titrate and rarely produces unexpected exaggerated response, does not reduce perfusion to placenta, ideal solution to correct sympathectomy induced hypovolemia and decr SVR • CONS: • Efficacy is reduced when NE stores are depleted • Risk of malignant hypertension if used with MAOi • Tachyphylaxis with repeat doses
Vasopressors • Norepinephrine • Primary postganglionic sympathetic neurotransmitter • Direct alpha 1&2 and beta-1 • Starting Dose .05-.5 mcg/kg/min IV infusion via central access only • PROS: • Direct agonist, redistributes blood flow to the brain and heart because all other vascular beds are constricted • CONS: • Reduced organ perfusion: risk of ischemia to kidneys, gut, liver, skin and extremities, causes pulmonary vasoconstriction, arrhythmias, and possible skin necrosis with extravasation
Vasopressors • Epinephrine • Catecholamine produced by the adrenal medulla • Direct alpha 1&2, and beta 1&2 • Peripheral vasoconstriction increases diastolic pressure • PROS: • Direct acting, potent alpha and beta activity gives max effects and give equivalent increases in SV, less tachycardia after heart SX than other ionotropes, effective bronchodilator • CONS: • Tachycardia and arrhythmias, potential organ ischemia including MI, increases PVR
Vasopressors • Dopamine • Direct alpha 1 and beta 1&2… and dopaminergic agonist • Indirect action : releases stored NE • Pros: • increases renal perfusion and urine output at low doses, BP response is easy to titrate due to its mixed vasopressor/inotropic effects • Cons: • response can diminish when NE stores depleted, sinus/atrial/ventricular tachycardia or arrhythmias may occur, max inotropic effect less than epi, skin necrosis may occur w/ extravasation, MVO2 increases, and MI may occur if coronary blood flow doesn’t increase simultaneously, incr BP at higher doses may be detrimental to failing heart
Vasopressors • Dopamine
Vasopressors • Vasopressin • Endogenous antidiuretic hormone that produces direct peripheral vasoconstriction thru V1 receptors • Pros: • effective in increasing SVR in severe acidosis, sepsis, and after CPB, cerebral vasodilator, may restore CPP after cardiac arrest without producing tachycardia • Cons: • Unpleasant symptoms in awake patients( abd cramping, uterine contractions, nausea, bronchoconstriction, skin pallor, incr liver enzymes and perfusion to gut with prolonged use, decr plts, lactic acidosis
Amiodarone and Lidocaine • Utilized to suppress ventricular ectopy • Lidocaine • Depresses automaticity by reducing slope of phase 4 depolarization • Amiodarone • Na, K, Ca, alpha, and beta blocking properties • Stabilizes atrial and ventricular membranes • Utilized in ACLS for refractory VF and dysrhthmias • May causes hypotension and bradycardia
Atropine • Vagolytic effect enhances sinus node automaticity and AV conduction • Sodium Bicarbonate • No longer routinely utilized in ACLS • Use restricted to arrest associated with hyperkalemia, pre-existing metabolic acidosis, tricyclic/phenobarbital • Cons: metabolic alkalosis, hypernatremia, hyperosmolarity • Calcium • Increases contractility and increases ventricular automaticity • CaCl produces higher and more consistent levels of ionized calcium than other salts