week 4- Adrenergic-Blocking Agents Flashcards
Adrenergic Blockers
Bind to adrenergic receptors, to inhibit or block stimulation of the sympathetic nervous system (SNS) (fight &flight response)
Alpha-blockers and beta-blockers
ADRENERGIC BLOCKERS Have the opposite effect of adrenergic agents
.
Also known as:
Adrenergic antagonists
OR
Sympatholytics
These drugs are antagonists –bind to adrenergic receptors to inhibit or block stimulation by epinephrine or norepinephrine (sympatholytics)
classified
Classified by the type of adrenergic receptor they block
Alpha 1
–Located on the cells, muscles, organs that the nerve is stimulating—post synaptic effector cells
Alpha 2
—Located on nerves that initiating the stimulation –pre synaptic effector nerve endings
Beta 1
—Primarily located on the heart
Decrease heart rate and blood pressure
Beta 2
—Located on smooth muscles of the blood vessels & bronchioles
Block the effects of the adrenergic receptors
The effects of the adrenergic blockers
differ depending on the cells or tissue that they exert their action on.
Adrenergic Blockers Used For:
Hypertension: causes vasodilatation of the blood vessels
Tachycardia: blocks stimulating effects
Cardiac arrhythmias: prevention of tachycardia, controlled stimulation
Angina: vasodilatation, decreased O2 consumption
Migraine headaches: vasoconstriction of cerebral vessels (ergotamine)
Uterine bleeding: causes vasoconstriction (ergotamine)
Labour uterine contraction: vasoconstriction (oxytocin)
Benign prostatic hyperplasia BPH: relaxation and dilatation of the vascular area and smooth muscle of the prostate
Glaucoma: vasodilatation
Prazosin (Minipress)
Cause both arterial and venous dilation, reducing peripheral vascular resistance and BP
Used to treat hypertension
Tamsulosin (Flomax) (specific for BPH)
Effect the receptors of prostate gland and bladder to decrease resistance of urinary outflow, thus reducing urinary obstruction and relieving effects of BPH (benign prostatic hyperplasia)
Ergot alkaloids
migraines
Phentolamine (Alpha Blocker)
Quickly reverses the potent vasoconstrictive effects of vasopressors such as norepinephrine or epinephrine
Restores blood flow and prevents ischemic tissue leading to tissue necrosis
Causes vasodilation
Alpha-Blockers: Side Effects
Palpitations, orthostatic hypotension, tachycardia, edema, dysrhythmias, chest pain
Dizziness, headache, drowsiness, anxiety, vertigo, weakness, numbness, fatigue
Incontinence, nosebleed, tinnitus, dry mouth, pharyngitis, rhinitis
Common Agents
phentolamine (Regitine)
reversal of vasoconstriction from epinephrine and norepinephrine
prazosin (Minipress)
for treatment of hypertension
tamsulosin (Flomax)
BPH (benign prostate hyperplasia)
ergotamine tartrate (Ergostat)
for uterine bleeding or heavy menstrual bleeding
Beta-Blockers
Block stimulation of beta-receptors in the SNS
Competes with norepinephrine and epinephrine
Beta Blockers can be either depending on the receptors they block:
Nonselective and selective beta-blockers
also called
Nonspecific or cardioselective beta-blockers
Beta1-receptors
Located primarily on the heart
Beta-blockers selective for these receptors are called cardioselective beta-blockers
Effective for cardiac arrhythmias and hypertension
Effects heart contractility, heart rate and conduction resulting in bradycardia, decrease contractility and decrease conduction
ie. atenolol, propranolol, metoprolol
Beta2-receptors
Located primarily on smooth muscles of bronchioles and blood vessels
Blocking bronchodilating effect from the smooth muscle causes relaxation - resulting in bronchoconstrition of the lungs
Use with caution in patients with lung disorders, asthmatics. Can worsen the effects and put the patient at risk for respiratory distress
Mechanism of Action -Cardioselective (beta1)
Reduce SNS stimulation of the heart
Decreases heart rate
Prolongs SA node recovery
Slows conduction rate through the AV node
Decreases myocardial contractility, thus decreasing myocardial oxygen demand
Peripheral pooling of blood due to relaxation of smooth muscles (Beta 2) leads to orthostatic hypotension
Mechanism of Action- Nonspecific (beta1 and beta2)
Effects on heart: Same as cardioselective
Bronchioles: Constriction, resulting in narrowing of airways and shortness of breath
Peripheral Vessels: Vasodilation
Side Effects: Beta-Blockers
AV block, bradycardia, heart failure, peripheral vascular vasodilation
Dizziness, lethargy
Nausea, vomiting, diarrhea, cramps
Impotence, rash, alopecia, bronchospasm
beta blockers types
Atenolol
-cardioselective, used to prevent future MI post MI, hypertension angina
Acebutolol
Used for hypertension, ventricular and supraventricular dysrhythmias and angina
Used immediate period post MI
Esmolol
Very potent, short acting, only IV, used in emergency situation for rapid temporary control of arrhythmias
Labetolol
Blocks both alpha and beta adrenergic receptors
Used for severe hypertension and hypertension emergencies to quickly lower BP
Metoprolol
Used in post MI pts
Propranolol
Non selective, first beta blocker agent
Used in the treatment of digoxin toxicity, tachyarrhythmias, hypertrophic sub-aortic stenosis, thyrotoxicosis, migraine headaches, adrenal tumors
Sotolol
Non-selective, very potent antidysrhythmic, treat arrhythmias—often for the more difficult arrhythmias, used as a cardioversion drug
alpha-blockers may precipitate hypotension
Remember that some beta-blockers may precipitate bradycardia, hypotension, heart block, HF, and bronchoconstriction
These medications should never be stopped abruptly
.
Beta-Blocking Agents: Nursing Implications
Patients should report the following to their physician:
Weight gain of more than 2 pounds (1 kg) within a week Edema of the feet or ankles Shortness of breath Excessive fatigue or weakness Syncope or dizziness
antagonists vs agonists
agnoist drugs stim the SNS because the bind to the receptor and cause a response.
antagonists inhibit or block stimulation of the SNS
a-BLOCKERS at the a receptors leads to
vasodilations, decrease in BP, miosis, and supressed ejaculation
oxytocics
drugs given postpartum and postabortion to control bleeding
beta (b1) blockers result in
(LOCATED IN THE HEART*****)
REDUCES HEART RATE, SLOWS CONDUCTION THROUGH AV NODE, PROLONGS SA NODE, AND CONTRACTILITY.
so in short,decreases conduction, contraciliity, and heart rate
SOME B-BLOCKERS ARE MAINLY USED TO TREAT
ANGINA
VASODILATION OF BLOOD VESSELS WITH THE A-BLOCKERS RESULT IN
A DROP IN bp and increase in urinary flow rates.
blocking b2 receptors leads
to decrease in in bronc smooth muscle relaxation, or broncoconsrtiction
- Beta blockers are used in the treatment of
HYPERTENSION, DYSRYTHMIAS and GLAUCOMA, HEART RATE AND MIGRANES
- Rebound hypertension with chest pain can be seen if
STOPPED ABRUTPLY MEDS
Shortness of breath, pitting edema, syncope, dizziness, fatigue and weakness are symptoms of
CONGESTIVE HEART FAILURE
with a-blockers the predominate response is
vasodilation. this response is due to blocking of the a-adrenergiceffect of vasoconstriction, which results in blood vessel dialtion
vasodilation of blood vessel with the a-blockers will result in
BP drop and reduction in urinary obstruction that may lead to increase urinar flow rates.
