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There are three known types of beta receptor, designated β1, β2 and β3. β adrenergic receptor are all located on postsynaptic effector cells. The β₁- adrenergic receptors are located in the heart and kidney; β₂-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β₃- receptors are located in fat cells.
B E T AA D R E N E R GI
SUBMITTED BY: MARA VIVIENNE DOCTOR- HERRERA BSN IV-1 OSP
Beta-adrenergic blocking agents, beta-adrenergic or beta antagonists may also referred to as beta- blockers. (sometimes written as β-blocker). Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction, dilation of blood vessels and opening of bronchi, and also reduce tremor and breakdown of glycogen. It is therefore expected that non-selective beta blockers have an antihypertensive effect. The antihypertensive mechanism appears to involve reduction in cardiac output (due to negative chronotropic and inotropic effects), reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity (for those β-blockers that do cross the blood-brain barrier, e.g. Propranolol).(1) The nonselective beta-blockers, including propranolol, oxprenolol, pindolol, nadolol, timolol and labetalol, each antagonize both b1 - and b2-adrenergic receptors. For the selective antagonists, including metoprolol, atenolol, esmolol, and acebutolol, each has much greater binding affinity for the b1 adrenergic receptor. The selective beta-blockers are normally indicated for patients in whom b2-receptor antagonism might be associated with an increased risk of adverse effects. Such patients include those with asthma or diabetes, or patients with peripheral vascular disease or Raynaud's disease. (2) Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. Negative chronotropic properties of beta blockers allow the lifesaving property of Heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states. The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade. Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium and water retention.(1)
Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin release.
Stimulation of β2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of β3 receptors induces lipolysis. (1) There are no general pattern in the degree and/or direction of stereoselectivity among different beta-blockers. This is perhaps because β-adrenergic antagonists encompass a wide spectrum of pharmacokinetic properties, with low to high degrees of plasma protein binding, extent of excretion into urine as unchanged drug, and hepatic extraction ratios. Additionally, the degree and direction of stereoselectivity in the pharmacokinetics of these drugs are susceptible to change because of patient and/or disease characteristics. Because of the significant enantioselectivity in the pharmacologic effects of beta-blockers, a stereoselective change in the pharmacokinetics of these drugs may be associated with an altered pharmacodynamic profile. (2) The pharmacokinetics of beta-blocking drugs can also be influenced by race, age, cigarette smoking and concomitant drug therapy. The wide interpatient variability in plasma drug concentration observed with beta-blockers makes this parameter unreliable in routine patient management. Despite the pharmacokinetic differences among the beta-blockers, these drugs should always be titrated in the individual patient to achieve the desired clinical response. (3)
β – adrenergic blockers also have a profound effect on the conduction system of the heart. The AV node normally receives impulse stimulation from the SA node and slows it down so that the ventricles have time to fill before they are stimulated to contract. Conduction in the SA node, which spontaneously depolarizes at the most frequent rate, is slowed by β – adrenergic blockers, which results in a decreased heart rate. These drugs also slow conduction through the AV node. These effects of β – adrenergic blockers on the conduction system of the heart make them useful drug in the treatment of various type of irregular heart rhythms, called dysrhythmias. Their ability to reduce SNS stimulation of the heart, including reducing heart rate and the force of myocardial contraction (systole), renders β – adrenergic blockers useful in treating hypertension. Traditionally β – adrenergic blockers were thought to worsen heart failure. However, recent studies have shown benefit to the use of β – adrenergic blockers. Certain β – adrenergic blockers such as carvedilol and metoprolol have produced the best results to date. The form of heart failure that includes a diastolic dysfunction component responds especially favorably to β – adrenergic blockers.(4)
Beta blockers are a class of drugs used for various indications, but particularly for the management of • • • cardiac arrhythmias, cardioprotection after myocardial infarction (heart attack), hypertension.
Other Indications for beta blockers include: • • • • • • • • • Angina Mitral valve prolapse Atrial fibrillation Congestive heart failure Glaucoma Migraine prophylaxis Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism Essential tremor Phaeochromocytoma, in conjunction with α-blocker (1)
1. Administer oral beta-blocker before meals and at a.m. If insomnia occurs. 2. Check client’s apical pulse rate before drug administration, refer if below 60bpm. 3. Hypotensive precautions 4. Warn clients not to drive or operate dangerous machinery until he/she has adjusted to medications.(5) 5. Monitor vital signs and pulse, observe for signs of bradycardia, heart failure, orpulmonary edema. (Beta-blockers decrease heart rate and cardiac output.)
6. Monitor for orthostatic hypotension. (Beta-blockers cause orthostatic hypotension.) 7. Observe for drowsiness, fatigue, and weakness. (These are side effects of betablockers.) 8. In diabetic clients, monitor for hypoglycemia. (Some beta-blockers may lower blood glucose levels.) 9. Monitor for effects on the heart, especially with exertion. (Beta-blockers can decrease cardiac output.)(6)
DRUG ACEBUTOL OL (Sectral) ATENOLOL (Tenormin) DOSE/ ROUTE OF ADMINISTRATION ADULT: PO:400-800 mg/day 600-1200 mg/day divided bid ADULT: PO: 50-100 mg/day daily or bid 50-200 mg/day or bid IV: 5 mg over 5 min; repeat in 10 min ADULT: IV: Bolus of 500 mcg/kg over 1 min, followed by 4 min at 50 mcg/kg/min and evaluate IV: 80 mg bolus over 30 min followed by 150 mcg/kg/infusion
NON- SELECTIVE AGENTS
PROPANOL OL (Inderal) ADULT: PO: 80-320 mg/day divided bid-qid 120- 640 mg/day divided bid- tid 10-30 mg tid-qid 20-40 mg tid/qid 120-320 mg/day divided 30-60 mg/day divided for 3 days before surgery with an α-blocker also IV: 1 mg slow IV push, may repeat every 5 min up to 5 mg
SOTALOL (Betapace) CARVEDILO L (Coreg)
ADULT: PO: 160-320 mg/day divided ADULT: PO: 3.125 mg bid; may double dose every 2wk to highest tolerated dose, max 50 mg/day
p.270-293, Liley, Harrington, Synder; Pharmacology and the Nursing Process; Fifth Edition; 2007.
SAMPLE OF (DRUG) IMAGES
Low Blood Pressure Asthma Low Blood Pressure Nausea Slow Heart Rate Headaches Impaired Circulation Dizziness Loss of Sleep Muscle Cramps Heart Failure Peyronie's disease
nausea abnormal vision
exacerbation of Raynaud's syndrome
erectile dysfunction and/or alteration of glucose
DOCUMENT REFERENCES: 1. http://en.wikipedia.org/wiki/Beta_blocker 2.http://www.ualberta.ca/~csps/JPPS4(2)/R.Mehvar/betablockers.htm 3.http://www.ncbi.nlm.nih.gov/pubmed/1674683 4. p.270-293, Liley, Harrington, Synder; Pharmacology and the Nursing Process; Fifth Edition; 2007. 5.http://www.scribd.com/doc/10455366/Pharmacology 6.http://wps.prenhall.com/wps/media/objects/3775/3866436/npf_charts/ch23/Betaadrenergic%20Antagonist.pdf
IMAGE REFERENCES: (WEB)
ACEBUTOLOL (Sectral) https://members.kaiserpermanente.org/kpweb/image/feature/026drugency/drugphotos/WYE 41790.JPG
ATENOLOL (Tenormin) http://ordertenormin.org/images/tenormin.jpg https://members.kaiserpermanente.org/kpweb/image/feature/026drugency/drugphotos/ZNC 01050.JPG ESMOLOL (Brevibloc) http://www.frca.co.uk/images/esmolol.jpg
PROPANOLOL (Inderal) http://www.aclepsa.com/images/prescriptions/inderal_tn.jpg http://www.drugs.com/images/pills/mmx/t103963f/inderal_la.jpg SOTALOL (Betapace) http://www.peacehealth.org/kbase/media/medical/multum/betapace160mg.jpg CARVEDILOL (Coreg) http://www.patentlyo.com/patent/081208_0235_NoInequitab1.jpg http://www.drugs.com/images/pills/mtm/Coreg%2012.5%20mg.jpg VISIT:
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