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 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 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 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 Dose(mcg/kg/min) Receptors Activated SVR 0.01-0.03 Beta May decrease 0.03-0.15 Beta >alpha Variable 0.15-0.5 Alpha 1 + Beta Increased

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 Dose (mcg/kg/min) Receptors Activated Effect 1-3 Dopaminergic (DA1) Increased renal & mesenteric blood flow 3-10 Beta 1 & 2 (plus DA1) Incr HR, CO, contractility, and PVR decreased SVR >10 Alpha (plus beta&DA1) Increased SVR, PVR,HR, arrhythmias Decreased renal blood flow and poss CO

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 Sodium Bicarbonate Calcium 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