Transcript Vasopressors

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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
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Activation of alpha-2
◦ Presynaptic receptors decreases NE release thru negative
feedback
 Brain receptors lowers the blood pressure (decreases SNS
activity) and causes sedation
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Beta-1
◦ Located primarily on post synaptic membranes of
the heart
 Positive chronotrope, dromotrope, and inotrope
◦ Fat Cells: Lipolysis
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Beta – 2
◦ Located primarily on post synaptic smooth muscle
and gland cells
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Blood Vessels: Vasodilation
Bronchioles: Bronchodilaton
Uterus: Relaxation of uterus
Kidneys: Renin Secretion
Liver: Gluconeogenesis, glycogenolysis
Pancreas: Insulin secretion
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Dopamine-1
◦ Blood Vessels: Dilates renal, coronary, and
splanchnic vessels
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Dopamine-2
◦ Presynaptic endings: inhibits NE release
◦ CNS: Psychic disturbances
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Phenylephrine
◦ Primarily direct alpha-1 agonist with minimal beta
affects
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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
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Ephedrine
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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
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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
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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
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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
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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
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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
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Utilized to suppress ventricular ectopy
Lidocaine
◦ Depresses automaticity by reducing slope of phase
4 depolarization
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Amiodarone
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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
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Atropine
◦ Vagolytic effect enhances sinus node automaticity
and AV conduction
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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
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Calcium
◦ Increases contractility and increases ventricular
automaticity
◦ CaCl produces higher and more consistent levels of
ionized calcium than other salts