W1_CaseStudy_Kattakayam_Jaya (1)
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Advanced Pharmacology
Jaya Aju Kattakayam
South University
NSG6005
Dr Olson
December 2, 2023
2
Advanced Pharmacology
A 58-year-old post Myocardial infarction and angioplasty started on metoprolol for hypertension.
He has a history of coronary artery disease, diabetes, asthma, and hypertension.
The 2020 International Society of Hypertension Global Hypertension Practice Guidelines – recommend the use of selective ß1-receptor agonists in patients diagnosed with coronary heart disease, hypertension diabetes, and asthma. American Heart Association - https://www.ahajournals.org/doi/epub/10.1161/HYPERTENSIONAHA.120.15026 Clinical guidelines also help us to determine the best medication for patients with heart disease, and comorbidities like asthma, diabetes, and hypertension.
Q 1: Metoprolol is a cardioselective ß1-adrenergic receptor antagonist, primarily blocking the ß1 receptors in the heart (Rosenthal & Burchum, 2020). This selectivity helps reduce the heart rate and blood pressure by blocking the effects of catecholamines adrenaline and
noradrenaline specifically on the heart.
Beta-blockers bind with beta-adrenergic receptors, competing with catecholamines causing negative chronotropic and ionotropic effects. By blocking ß1 receptors in the juxtaglomerular cells, ß blockers lower blood pressure by decreasing
the activity of the renin-angiotensin activation system (Martínez et al., 2023).
There are three types of β-adrenoceptors, β
1
-, β
2
- and β
3
-adrenoceptors. Beta
1
-
adrenoceptors are found mainly in the cardiac muscles and stimulation of catecholamines causes positive chronotropic and ionotropic effects (Bennett et al., 2021). Beta
2
-adrenoceptors are present in bronchial smooth muscle, cardiac, and skeletal muscle, and blood vessels. Beta
3
-
adrenoceptors are seen in bladder muscles and adipose tissue (Bennett et al., 2021). Different hormones act on different β-adrenoceptors. Binding with Beta
1
-adrenoceptors, catecholamines like norepinephrine and epinephrine increase cardiac automaticity and velocity of conduction.
3
Beta-1 receptors also cause the release of renin from the kidneys. Catecholamines binding to beta-2 receptors induce smooth muscle relaxation and increased metabolic effects like glycogenolysis.
Beta-receptor antagonists or beta blockers block the effects of epinephrine and norepinephrine by binding to beta-receptors, reducing the availability of these receptors through competitive inhibition (Martínez et al., 2023). Beta-blockers bind to the beta-1 and beta-2 receptors, inhibit the chronotropic and inotropic effects, and the heart rate and force of contraction slow down. Beta-blockers also decrease blood pressure by decreasing renin and reducing cardiac output. The negative chronotropic and inotropic effects relieve angina symptoms by decreasing cardiac oxygen demand. Beta-blockers also prolong the atrial refractory
periods and cause a potent antiarrhythmic effect (Martínez et al., 2023). Metoprolol is a second generation β blocker, which does not cause β2 blockade at therapeutic doses but can block β2 receptors at higher doses (Rosenthal & Burchum, 2020). With minimal β2 blockade, metoprolol rarely causes adverse effects of bronchoconstriction and hypoglycemia.
Q 2: Metoprolol, second generation ß1-selective blockers, and cardioselective beta-
blockers exert several cardiovascular effects.
By blocking ß1 receptors in the myocardium, metoprolol lowers the heart rate and reduces the force of contraction. Metoprolol, by blocking ß1
receptors in the heart, decreases the velocity of AV node conduction. Metoprolol reduces cardiac
output, leading to a decrease in blood pressure. It also reduces blood pressure by decreasing the renin secretion by the kidneys and reducing peripheral vascular resistance. Metoprolol decreases the oxygen demand of cardiac muscles by blocking ß1 receptors in the heart. It increases exercise tolerance by decreasing the intensity and frequency of angina and reducing the risk of death in post-myocardial infarction patients. However, metoprolol is not
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effective for vasospastic angina (Rosenthal & Burchum, 2020). Metoprolol decreases the afterload by reducing the arterial pressure, further decreasing myocardial oxygen demand. By blocking ß1 receptors, metoprolol increases the oxygen supply to cardiac muscles, by increasing the time of diastole, when the myocardial vessels are perfused (Rosenthal & Burchum, 2020).
With minimal β2 blockade, metoprolol rarely causes adverse effects of bronchoconstriction and will not increase airway resistance. Also, metoprolol does not cause β2 blockade at therapeutic doses, so less likely to mask symptoms of hypoglycemia in diabetic patients. Thus, metoprolol is preferred over nonselective β blockers for the treatment of angina, myocardial infarction, and heart failure in diabetic and asthmatic patients (Rosenthal & Burchum, 2020). Patients on vasodilator therapy with nitroglycerin can benefit from β blocker to prevent reflex tachycardia (Rosenthal & Burchum, 2020). β blockers are also effective in preventing hypertension in pheochromocytoma. Non-cardiovascular benefits of beta blockers include decreasing intraocular pressure, making it effective for glaucoma treatment, reducing symptoms of hyperthyroidism and is also effective for migraine management (Rosenthal & Burchum, 2020).
Q 3: Metoprolol undergoes extensive first-pass metabolism in the liver (Rosenthal & Burchum, 2020). Metabolism, also called biotransformation, is the enzymatically mediated alteration of a drug structure. The primary site of metabolism of metoprolol is the liver, where it is metabolized by the cytochrome P450 enzyme system, particularly the CYP2D6 isoenzyme (Blake et al., 2013; Berger et al., 2018).
Q 4: Providers should take extra caution when prescribing beta blockers, including metoprolol, in patients having a history of asthma due to the potential for ß2-adrenergic receptor blockade. ß2 receptors are prevalent in the bronchial smooth muscle and blocking them can lead
5
to bronchoconstriction and worsening of asthma symptoms. However, cardioselective ß-blockers
(like metoprolol) may be considered with caution in asthma patients, as they have a higher affinity for ß1 receptors in the heart than ß2 receptors in the lungs.
Beta-blocker therapy and Asthma
Asthma patients have a double risk of developing cardiac diseases and stroke (Tuleta et al., 2017).
β
2
-agonist medications are the cornerstone in the management of asthma and lung diseases (
2020 GOLD Reports - Global Initiative for Chronic Obstructive Lung Disease - GOLD
, 2021). β-antagonists, also known as β-blockers, are the fundamental management of cardiovascular diseases (Unger et al., 2020).
Pharmacology
There are three types of β-adrenoceptors, β
1
-, β
2
- and β
3
-adrenoceptors. Beta
1
-
adrenoceptors are found mainly in the cardiac muscles and stimulation of catecholamines causes positive chronotropic and ionotropic effects (Bennett et al., 2021). Beta
2
-adrenoceptors are present in bronchial smooth muscle and in cardiac, skeletal muscle, and blood vessels. Beta
3
-
adrenoceptors are seen in bladder muscles and adipose tissue (Bennett et al., 2021). Propranolol, timolol, sotalol, etc. are non-selective beta-blockers inhibiting both β
1
- and β
2
-adrenoceptors. Metoprolol, atenolol, etc. are cardioselective β
1
-blockers with greater inhibition of β1-
adrenoceptors than β
2
-adrenoceptors. They are also called inverse agonists, causing a decrease in baseline receptor activity (Bennett et al., 2021). β-blockers can decrease the forced expiratory volume in 1 s (FEV
1
) causing bronchospasm in patients with asthma. With minimal β2 blockade,
metoprolol rarely causes adverse effects of bronchoconstriction and will not increase airway resistance. Also, metoprolol does not cause β2 blockade at therapeutic doses (Rosenthal & Burchum, 2020).
6
Safety concerns persist in using β-blockers for asthma patients. Bennett et al. (2021) studies proved that there is no evidence of asthma exacerbations in patients using β-blocker therapy.
For asthma patients who have a clinical indication like myocardial infarction and perceived benefit from a β-blocker, studies suggest that using β -blockers, at the least effective dose, will reduce the chances of bronchospasm (Bennett et al., 2021). Also, a mild decrease in lung function after the first doses in asthma patients was resolved with ongoing β-blocker therapy (Bennett et al., 2021). As Advanced Practice Registered Nurses (APRN), we should educate and encourage our patients. A diabetic and asthmatic patient started on metoprolol should be provided health education on asthma exacerbation chances, and masking hypoglycemia effect, and should be provided resources to contact the provider if they develop side effects. Patients should be educated about the adverse effects and how to detect and treat them early to provide the best outcomes.
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References
2020 GOLD Reports - Global Initiative for Chronic Obstructive Lung Disease - GOLD
. (2021, November 23). Global Initiative for Chronic Obstructive Lung Disease - GOLD.
https://goldcopd.org/gold-reports/
Bennett, M., Chang, C. L., Tatley, M., Savage, R., & Hancox, R. J. (2021). The safety of cardioselective β
1
-blockers in asthma: literature review and search of global pharmacovigilance safety reports.
ERJ open research
,
7
(1), 00801-2020. https://doi-
org.su.idm.oclc.org/10.1183/23120541.00801-2020
Berger, B., Bachmann, F., Duthaler, U., Krähenbühl, S., & Haschke, M. (2018). Cytochrome P450 enzymes involved in metoprolol metabolism and use of metoprolol as a CYP2D6 phenotyping probe drug.
Frontiers in Pharmacology
,
9
. https://doi.org/10.3389/fphar.2018.00774
Blake, C. M., Kharasch, E. D., Schwab, M., & Nagele, P. (2013). A meta-analysis of CYP2D6 metabolizer phenotype and metoprolol pharmacokinetics.
Clinical pharmacology and therapeutics
,
94
(3), 394–399. https://doi-org.su.idm.oclc.org/10.1038/clpt.2013.96
Martinez, A., Mohit, L., Sameep, M., Aslam, M. A., Anouksha, B., Shashwat, K., Reddy, S. S., Ahmed, S. S., Waleed, R., Susmitha, A., & Khawaja, U. A. (2023). Beta-Blockers and Their Current Role in Maternal and Neonatal Health: A Narrative Review of the Literature.
Cureus, 15
(8)
https://doi.org/10.7759/cureus.44043
Rosenthal, L., & Burchum, J. (2020).
Lehne’s Pharmacotherapeutics for advanced practice providers
. Saunders.
Tuleta, I., Skowasch, D., Aurich, F., Eckstein, N., Schueler, R., Pizarro, C., Schahab, N., Nickenig, G., Schaefer, C., & Pingel, S. (2017). Asthma is associated with atherosclerotic
8
artery changes.
PLOS ONE
,
12
(10), e0186820.
https://doi.org/10.1371/journal.pone.0186820
Unger, T., Borghi, C., Charchar, F. J., Khan, N., Poulter, N., Prabhakaran, D., Ramiréz, A. J., Schlaich, M. P., Stergiou, G. S., Tomaszewski, M., Wainford, R. D., Williams, B., & Schutte, A. E. (2020). 2020 International Society of Hypertension Global Hypertension Practice Guidelines.
Hypertension
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75
(6), 1334–
1357.
https://doi.org/10.1161/hypertensionaha.120.15026