Beta-adrenergic blockers: Nursing pharmacology

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BETA-ADRENERGIC BLOCKERS
DRUG NAME
carvedilol (Coreg), labetolol (Trandate), nadolol (Corgard), propranolol (Inderal, InnoPran XL), pindolol (Visken), sotalol (Betapace, Sorine)
atenolol (Tenormin), metoprolol (Lopressor, Toprol XL), nebivolol (Bystolic)
CLASS
Nonselective β-blockers
Selective β-blockers
MECHANISM OF ACTION
Block β receptors → prevent catecholamines (norepinephrine and epinephrine) from binding and activating them → decrease cardiac contractility, decrease conduction velocity through AV node, decrease heart rate, cardiac output, and blood pressure
INDICATIONS
  • Hypertension
  • Coronary artery disease; angina pectoris, myocardial infarction
  • Arrhythmias
  • Heart failure
  • Essential tremor
  • Glaucoma
  • Migraine prophylaxis
ROUTE(S) OF ADMINISTRATION
  • PO
  • IV
  • Opth
SIDE EFFECTS
  • Bradycardia
  • Hypotension
  • Fatigue
  • Dizziness
  • Bronchospasm and dyspnea
  • Headache
  • Depression
  • Hallucination
  • Insomnia and nightmares
  • Erectile dysfunction
  • Decreased libido
  • Hyperglycemia
  • Hypertriglyceridemia
  • Hyperkalemia
  • Hypoglycemia unawareness
CONTRAINDICATIONS AND CAUTIONS
  • Bradycardia
  • Hypotension
  • Decompensated heart failure
  • Second or third degree AV block
  • Asthma
  • COPD
  • Diabetes
  • Raynaud phenomenon
  • Severe hepatic or renal disease
NURSING CONSIDERATIONS: BETA-ADRENERGIC BLOCKERS
ASSESSMENT AND MONITORING
  • Baseline assessment
    • Vital signs
    • Orthostatic hypotension
    • Frequency and duration of angina attacks
    • Weight, lung sounds; presence of edema, dyspnea
  • Laboratory test results: renal and hepatic function tests, electrolytes, glucose, lipid panel
  • Diagnostic tests: ECG
  • Monitor
    • Heart rate, blood pressure, ECG
    • Evaluate therapeutic response; e.g., normalized blood pressure, decreased anginal pain, absence of heart failure symptoms
CLIENT EDUCATION
  • Change positions slowly
  • Do not abruptly discontinue medication
  • Self-monitoring of pulse, blood pressure
  • Lifestyle modifications
    • Dietary modifications; e.g., low sodium diet
    • Weight control
    • Regular activity as tolerated
    • Moderate alcohol intake
    • Smoking cessation
  • Clients with diabetes: recognize signs of hypoglycemia; e.g., fatigue, hunger and difficulty concentrating
    • Check blood glucose regularly
  • Report symptoms such as bradycardia, hypotension, hypertension, dyspnea, edema
Author: Hussein Alsa’di, MBBS
Illustrator: Robyn Hughes, MScBMC

Transcript

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Beta-adrenergic blockers, or just beta blockers, are a group of medications that are mainly used to treat cardiovascular conditions like hypertension, coronary artery disease and its manifestations like angina pectoris and myocardial infarction, as well as heart failure and arrhythmias. Beta blockers can also be used to treat essential tremor, glaucoma, and as prophylactic treatment of migraine attacks.

Now, beta blockers work by blocking beta receptors, of which there are three types, known as beta 1, which are mainly found in the heart and kidneys; beta 2, found in the lung bronchioles as well as the arteries of skeletal muscles; and beta 3, found in adipose tissue. So, beta blockers are classified into two main groups: nonselective and selective. Nonselective beta blockers can block both beta 1 and beta 2 receptors, and include carvedilol, labetalol, nadolol, propranolol, pindolol, and sotalol. On the other hand, selective beta blockers only block beta 1 receptors, and include atenolol, metoprolol, and nebivolol. In addition, carvedilol and labetalol also block alpha-adrenergic receptors found on vascular smooth muscle, which causes vasodilation, or widening of the blood vessels.

Now, another thing to keep in mind is that all beta blockers end in –lol (no joke). Also, they can be administered orally, intravenously, or even via the ophthalmic route.

Once administered, beta blockers block beta receptors, thereby preventing the catecholamines norepinephrine and epinephrine from binding and activating them. As a result, beta blockers decrease the sympathetic nervous system response.

Now, the main therapeutic effects of beta blockers come from the blockade of beta 1 receptors in the heart, which decreases heart contractility and slows the conduction through the atrioventricular or AV node. This helps decrease the heart rate, which ultimately decreases the cardiac output. In addition, the blockade of beta 1 receptors in the kidneys decreases the release of renin, which stimulates the adrenal glands to release aldosterone, which in turn acts on the kidneys to induce water and sodium reabsorption. So, with beta blockers, there will be less renin and aldosterone, which results in natriuresis, or water and sodium excretion, reducing blood volume.

Therefore, beta blockers effectively lower the cardiac preload and the blood pressure and can be useful for clients with hypertension. Now, when beta blockers decrease the heart rate, cardiac output, and blood volume, the net result is a decrease in the workload on the heart. This also makes them an appropriate choice for the treatment of heart failure. In addition, beta blockers help decrease the myocardial oxygen demand. This is particularly important in coronary artery disease, like angina pectoris and myocardial infarction.

Now, the most common side effects of beta blockers result from excessive blockade of beta 1 receptors in the heart, and these include bradycardia, hypotension, fatigue, and dizziness. In addition, beta blockers can cause neurological side effects like headache, depression, hallucination, and sleep problems, like insomnia and nightmares. Biologically male clients on beta blockers may also experience decreased libido and erectile dysfunction. Side effects can also result from blockade of beta 2 receptors, especially by the nonselective beta blockers, but also by the selective beta blockers when used in high doses. In the bronchi, this results in bronchoconstriction, or bronchospasm, which decreases airflow to the lungs and leads to dyspnea. Finally, beta blockers have shown to cause certain metabolic changes like hyperglycemia, hypertriglyceridemia, and hyperkalemia. Moreover, beta blockers can lead to hypoglycemia unawareness, where a client with diabetes develops hypoglycemia but does not experience the typical hypoglycemic symptoms mediated by epinephrine, like tachycardia, palpitations, tremor, and anxiety.

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