Non-Selecting Direct acting Adrenergic agonists Flashcards
ISOPROTERENOL (isuprel)
Beta 1 and 2 Agonist (NO EFFECT ON ALPHA RECEPTORS)
- EFFECTS:
–> decrease TOTAL PERIPHERAL RESISTANCE
–> INCREASE HR (arrhythmias
–> INCREASE Myocardial CONTRACTILITY
–> BRONCHODILATION
- USES: Bradycardia, A-V block, TORSADES DE POINTES
DOBUTAMINE (dubutrex)
Beta 1. Beta 2, Alpha 1 (MAINLY ACTS ON Beta1 at therapeutic dose)
EFFECTS:
–> positive inotropic effect on heart (B1)
–> positive chronotropic effect (SA node automaticity, A-V cond)
–> Total peripheral resistance not affected (alpha1 - Beta2 balance)
USES: short term tx of cardiac failure
ADVERSE EFFECTS:
–> excessive increase in BP and HR, increased ventricular response rate, ventricular ectopic acitivty, may increase size of MI
–> Tolerance may develop (SHORT TERM USE)
EPINEPHRINE (Adrenaline)
- Potent ALPHA and BETA RECETPOR STIMULANT
- Dose/administration route-dependent
- SUBCUTANEOUS: Slow absorption and causes vasoconstriction
describe the dose responses to intravenous epinephrine
- SMALL DOSE: (DECREASE MAP)
–> Beta 1 = Increase pulse pressure (PP), Increase HR, SV, CO
–> Beta 2 = Decrease total peripheral resistance
- MODERATE DOSE: (increase MAP)
- -> Beta 1 = increase HR, SV, CO, PP
–> Beta 1 = Decrease TPR, DBP
–> Alpha 1 = INCREASE TPR, BP
- HIGH DOSE: (INCREASE MAP, BP)
–> Alpha 1 = INCREASE TPR, BP
–> potential reflex bradycardia
–> Beta 1 and 2 = lesser effects
describe the Vascular effects of epinephrine
- MAIN SITE of ACTION = SMALLER ARTERIOLES and PRECAPILLARY SPHINCTERS
- CAUSES A REDISTRIBUTION OF BLOOD FLOW
–> cutaneous blood flow DECREASES
–> Skeletal muscle blood flow INCREASES
–> Renal blood flow DECREASES; FF INCREASES, RENIN SECRETION INCREASES (Beta1)
–> pulmonary blood flow: PAP and PVP INCREASES
–> coronary blood flow INCREASES
–> Cerebral circulation has LITTLE EFFECT AT THERAPEUTIC DOSE
Describe the epinephrine reversal phenomenon
- alpha receptor antagonism causes INCREASE epinephrine induced VASODILATION –> DECREASE TPR –> DECREASE MAP
- Beta receptor antagonism –> Ephinephrine induced vasoconstriction unmasked –> INCREASE MAP
describe the cardiac effects of epinephrine
- POWERFUL CARDIAC STIMULANT (Beta 1)
- Heart rate INCREASES, shorted systole, diastole lengthens
- Increase Inotropy, lusitropy and chronotropy RESULTING IN INCREASE MYOCARDIAL OXYGEN CONSUMPTION
- Increase automaticity –> potential arrhythmias
describe the toxicity and adverse effects of epinephrine
- thobbing headache, tremor, and palpitations
- cerebral hemorrhage (large doses, rapid IV)
- Cardiac arrhythmias
- angina in patients with coronary artery disease
CONTRAINDICATIONS
–> PATIENTS USING NONSELECTIVE BETA BLOCKERS (cause severe vasoconstriction (epinephrine reversal)
what are the therapeutic uses of epinephrine
- Hypersensitivity reactions, including anaphylaxis
- cardiac arrest
- ingredient in local anesthetics
- post-extubation croup, viral croup
describe properties of Norepinephrine
- equipotent to epinephrine in stimulating BETA 1 RECEPTORS
- POTENT ALPHA AGONIST (mroe so than epinephrine)
- LITTLE ACTION ON BETA 2 RECEPTORS
describe the effects of norepinephrine
- INCREASE Systolic BP, Diastolic BP, PULSE PRESSURE
- INCREASE CORONARY FLOW (coronary dilation + elevated BP)
- unchanged/decreased cardiac output (decreased HR overcoming increased stroke volume
- INCREASE TOTAL PERIPHERAL RESITSANCE (TPR)
- Decrease renal blood flow
- decrease splanchnic and hepatic blood flow
- USES: tx of LOW BLOOD PRESSUE
describe the toxicity/adverse effects of norepinephrine
- same as epinephrine
–> restlessness, headache, tremor, palpitations
–> cerebral hemorrahge
–> cardiac arrhythmias
- angina in patients with coronary artery disease
- GREATER ELEVATION OF BLOOD PRESSURE
DOPAMINE
D1, D2, Beta 1 and alpha 2
- immediate metabolic precursor of norepinephrine and epinephrine
- in CNS: NT particularly important in the regulation of movement
- in periphery: synthesized in epithelial cells of the proximal tubule –> local diuretic and natriuretic effects
- is a substrate for both MAO and COMT –> ineffective when administered orally
Describe Dose response of DOPAMINE
- LOW DOSE:
–>Presynaptic D2 receptor = Decrease NE release and alpha adrenergic stim
–> Vascular D1 receptors = vasodilation (incrase GFR, RBF) –> decrease Na reabsorption
–> Renal tubular cell (D1) = Increase Na Filtered
–> END RESULT Na+ Diuresis
- MODERATE DOSE
–> POSITIVE INOTROPIC EFFECT (Beta 1)
–> NEGATIVE Systolic BP and pusle pressure
–> Total peripheral resistance UNCHANGED
- HIGH DOSE
–> GENERAL VASOCONSTRICTION (alpha 1)
Adverse reaction/ precautions of DOPAMINE
- Hypovolemia should be corrected before dopamine use
- Tachycardia, anginal pain, arrhythmias, headache, hypertension
- Extravasation –> Ischemic necrosis and sloughing
- MAO inhibitor or tricyclic antidepressant: avoid DOPAMINE or use extreme caution
–> MAO inhibitors will inhibit degradation of dopamine
USE of DOPAMINE
USED TO TREAT:
–> Severe congestive heart failure, particularly in patients with oliguria and low or normal peripheral vascular resitsance
–> cardiogenic and septic shock
–> may acutely improve cardiac and renal function in severely ill patietns with chronic heart disease or renal failure
What are the effects of treating with reserpine or guanethidine prior to giving direct acting adrenergic agonists
- RESPONES OF DIRECT ACTING ADRENERGIC AGONISTS are NOT REDUCED BY PRIOR TX WITH RESERPINE OR GUANETHIDINE
- response may be potentiated by cocaine, reserpine and guanethidine
