Catecholamines Flashcards
Epinephrine
endogenous catecholamine
non- selective adrenergic agonist
directly stimulates Alpha and Beta receptors
-lower dose; 1 - 2 mcg/min; B2 stimulation
-moderate dose; 4 - 5 mcg/min; B1
-larger dose 10 - 20 mcg/min alpha and beta
Direct acting; via G protein receptor binding
change in intracellular Ca = agonist effect
Uses;
- increases contractility, BP and HR
- maintains CA blood flow
- Bronchospasm
- Bronchodilation –> B1
- Decrease Bronchial secretions –> Alpha
- Anaphylaxis
- ACLS [[ 1 mg q 3 - 5 min for arrest]]
- Prolongs LA DOA –> B1
- smooth muscle dilator [[low dose]]
- decreases SVR and decrease DBP [[beta 2 effects]]
- vasoconstrictor; decreases BF to renal and splanchnic
- increases BP, CVP and cardia work
- Decrease Histamine release
MOA;
How it works; Increases cAMP activity via G protein receptor binding
- change in intracellular Ca = agonist effect
Doses; ACLS; 1 mg q 3 - 5 min for arrest low dose; 1 - 2 mcg/min [[B2 stim]] moderate dose; 4 - 5 mcg/min [[B1 stim]] large dose; 10 - 20 mcg/min [[A &; B stim]]
Pharmacokinetics Onset; 1 - 2 min E1/2 time; 30 seconds DOA; 5 - 10 min Metabolism and Elimination; -reuptake/ diffuse away -COMT -MAO metabolite; vanillylmandelic acid (VMA)
Side Effects
- Tachycardia
- Angina
- Arrhythmias
- HPTN/ increased SVR
- increased IOP
- vasoconstriction of skin, GI, muscles, liver, kidney
- gangrene in digits
- hyperglycemia
- headache
- decreases LA absorption [[increased DOA]]
- decreases Uterine Blood Flow
Contraindications;
avoid in peripheral blocks and shock
caution in Dm, CAD, MAOI, pheochromocytoma, glaucoma and hyperthyroidism
pregnancy caution; decreases Uterine blood flow
Norepinephrine
- Direct acting
- endogenous catecholamine
- adrenergic agonist
dose;
low dose increase BP & C0
4 - 16 mcg/min
0.01 - 0.1 mcg/kg/min
Direct acting; α; B1 > > >B2
- acts on G-protein coupled receptor
- influx of Ca causing agonist effect and increase contractility
Uses;
- normal C0 with low SVR and BP
- caution in cardiogenic shock - potent vasoconstrictor
- increases SVR
- maintains coronary and cerebral blood flow when BP decreased
- improves renal and splanchnic blood flow (if volume resuscitated)
How it works; acts on g-protein to increase cAMP activity
-influx of Ca causing agonist effect and increased contractility
Pharmacokinetics; onset; rapid E1/2 time; 2.5 min DOA; 5 -10 min Metabolism & Elimination - reuptake or diffuses away -MAO -COMT metabolite; vanillylmandelic acid (VMA)
Side Effets;
- increase SBP &; DBP &; MAP
- decrease HR r/t baroreceptor reflex
- decreased RBF &; HBF and splanchnic
- organ ischemia
- extravasation produces encores [[ tx w/ phentolamine]]
Contraindicated;
- Hypovolemic
- Pheochromocytoma
- Thyroid storm
- Thrombosis
- MAOI & TCA
caution in renal and liver disease
Dopamine
-endogenous catecholamine
-adrenergic agonist
-precursor of NE; extracted from L- dopa in catecholamine synthesis of tyrosine
-directly stimulates dopa receptors;
D1 = D2»_space; B»_space; A
-high doses also have indirect effect and release endogenous NE
MOA; via G-protein coupled receptor leading to vasodilation and indirect effects of endogenous NE release
Dose;
D1; Low Dose; 0.5 - 2 mcg/kg/min
Beta; Medium Dose; 2 - 5 mcg/kg/min
Alpha; Large Dose; >10 mcg/kg/min
Uses;
- Vasodilation; ↑cAMP activity in vascular smooth muscle
- ↑ CO/ contractility
- ↑ RBF, ↑UO, ↑GFR [[most renal safe]]
- Synergistic with Dobutamine*
- ↑CO and decreases SVR
Dopa; Vasodilation [[Renal]]
Beta; Contractility [[increased CO and force of heart contraction
Alpha; Vasoconstriction [[all organs and smooth muscle]]
high doses –> mainly alpha effect which is vasoconstriction of all organs and smooth muscle [[decreased RBF]]
Pharmacokinetcs; onset; rapid E1/2 time; 1 min DOA; 5 -10 min Metabolism and Elimination; -25% becomes NE [[precursor for NE]] -75% MAO; COMT
Side Effects;
Tachycardia
-Arrhythmias
-Angina
-↑IOP
-↑UOP
-N/V; activates chemo receptor trigger zone in brain
-extravasation can cause necrosis [[tx w/ phentolamine]]
-inhibits carotid body; alters hypoxia repose
synergistic with dobutamine to ↑CO and decreases SVR
Contraindicated
- Pheochromocytoma
- Thyroid Storm
- MAOIs
Caution in;
- CAD
- Right Heart Failure
- Sulfa allergy
Dobutamine
-synthetic catecholamine
-synthetic analog of isoproterenol (which is made from dopamine)
-sympathomemetic
-Beta 1 selective agonist
B1 > B2»_space;»a
MOA; B1 >B2»_space;»a
- B1 selective [[not at SA node; no change in HR and BP]]
- acts on B1 G-protein receptor increases cAMP
- influx of calcium causes increased contractility and CO
- some B2 vasodilation that decreases SVR
Dose;
initial; 1 - 2mcg/kg/min
titrate up; 2 - 20mcg/kg/min
MAX; 40 mcg/kg/min
Uses;
- short term inotropic support
- improve CO inpatients with cardiac decompensation r/t decreased contractility
- cardiogenic shock
- CHF
- improves CO without increasing HR and BP
- Coronary Artery vasodilation
- Synergistic with dopamine to distribute CO
- synergistic with other pressors to decrease after load
- good for heart failure
- beta 1 selective; not at SA node; no change in HR and BP
Pharmacokinetics; Onset; 1 - 2 min E1/2 time; 2 min DOA; 5 - 10 min Metabolism and Elimination ; -reuptake of diffuse away -MAO -COMT
Side Effects;
- minimal HR increase (B1 selective increase CO without change in HR and BP)
- Arrhythmias
- Dyspnea
- Angina
- HTN
- Minimal decrease SVR
- Platelet inhibition
- Thrombocytopenia
Contraindications;
Avoid in;
-IHSS (idiopathic hypertrophic sub-aortic stenosis)
-MAOI and TCA
Caution in;
- CAD (risk of ischemia)
- MI (increase 02 demand)
- hypovolemia
- sodium bisulfate sensitivity
Isoproterenol
- synthetic catecholamine
- sympathomimetic
MOA:
- Binds to Beta receptors and activates G-protein; increases cAMP activity; influx of Ca causing B1 inotropy and chronotropy & B2 vasodilation
- pulmonary and systemic vasodilator
B1=B2»>a
B1; isotropy/ chronotropy of heart [[chemical pacemaker]]
B2; relaxation of pulmonary, GI and uterine
Dose; 0.5 - 10 mcg/min
Uses;
- Chemical Pacemaker; used for pacemaker failure
- 3rd degree heart block
- chronotropic agent after heart transplant
- Bradycardia/ refractory bradycardia
- emergency tx for arrhythmia, heart block and shock
- Beta Blocker OD
- Pulmonary and systemic vasodilator
Pharmacokinetics; onset; Rapid E1/2 time; 3 - 5 min DOA; 5 - 10 min Metabolism and Elimination; -COMT in liver and lungs -50% eliminated unchanged in kidneys
Side Effects;
- Tachycardia
- Arrhythmias
- decreased Coronary BF r/t decreased DBP (vasodilation)
- hypotension
- increased 02 demand (incased HR and contractility)
Contraindications;
- CAD
- Phenochromocytoma
- Thyroid Storm
- Hypersensitivty
- MI
- IHSS (idiopathic hypertrophic sub-aortic stenosis)
- Tachycardia caused by Dig toxicity
Phenylephrine
-synthetic NON-catecholamine
-direct acting
-selective alpha 1
A1> A2»>B
MOA; selective A1 agonist with –direct stimulation of the A1 adrenergic receptor and activates G-protein, increasing phospholipase C activity, increased Ca –> vasoconstriction
Venous > arterial constriction
Dose; IV bolus 50 - 200mcg q 5 min
IV maintenance infusion 20 - 50mcg/min
(double dilute)
Uses;
- tx systemic hypotension and maintenance of BP in patients with normal CO and HR
ex. vasodilation after general, epidural or spinal anesthesia induction - prevent epistaxis with nasal airway/ intubation
- Prolong DOA of LA
- Tx WIDE angle glaucoma
- Tx SVT
*directly stimulates Alpha 1
Veno > Arterial vasoconstriction
- Increases MAP, SBP, DBP, and SVR,
- decreases HR
Pharmacokinetics; Onset; <1 min E1/2time; 3 hours [[longer if long term infusion]] DOA; 5 - 20 min Protein binding; 90% highly protein bound Metabolism and Elimination; -MAO [[liver]] -90% eliminated unchanged in urine
Side Effects;
- Bradycardia
- Arrhythmias
- MI
- Hypertension
- decreased CO
- decreased renal and splanchnic blood flow
- decreased UOP
- rebound nasal congestion
- metabolic acidosis
- extravasation/ necrosis
Contraindications;
- WIDE angle glaucoma
- CHF
- Arrhythmias
- Severe HPTN and tachycardia
- hypersensitivity
- MAOIs, TCAs, Cocaine
caution; elderly, heart block, HPTN and bradycardia
Ephedrine
- synthetic NON catecholamine
- Direct AND Indirect adrenergic agonist
- Alpha = Beta
- 250x weaker than epi but lasts 10x longer
MOA; stimulates Alpha and Beta receptors directly and indirectly; mostly indirect stimulation
- directly stimulates A and B receptors; activates G-Protein; increases cAMP activity; Ca influx, increases contractility and vasoconstriction (venous >arterial)
- indirectly increases release of endogenous NE that stimulates receptors
Dose; 5 - 25mg
Uses;
- increase systemic BP to tx hypotension from SNS blockade caused by regional, inhales or IV anesthesia
- symptomatic bradycardia from anesthesia
- Post op NV from postural hypotension
- bronchodilator
- hypotension from VAE
- increases BP, HR, CO, preload, BF to muscles and CA
- decreases BF. to renal and splenic
*indirectly works on A and B by stimulation endogenous release of NE
*directly works on A and B
increases myocardial contractility (increased BP, C), HR and coronary and skeletal muscle BF), increases preload Venous >arterial constriction
decreases Renal and splenic BF
Pharmacokinetics; onset; rapid E1/2 time; 3 hrs DOA; 1 - 1.5 hours (inactivation is slow) Metabolism and Elimination -RESISTANT to MAO -inactivation is slow -40% eliminated unchanged in the urine
Side Effects
- TachyPHYLAXIS
- Arrhythmias
- HPTN
- MI
- increased CO
- CNS stim
- decreased uterine BF
Contraindicated;
- CAD
- MAOIs and TCAs and cocaine
- caution in trauma; or anyone with depleted catecholamine stores (indirect effects rely on NE stores)
- hypersensitivity
