Nurse practitioners (NPs) play a crucial role in the management of cardiovascular conditions

Week 2 lesson

Nurse practitioners (NPs) play a crucial role in the management of cardiovascular conditions. This includes selecting the most appropriate medication based on a client’s specific health profile and adjusting medication regimens accordingly. The therapeutic management of hypertension, arrhythmias, and chronic coronary diseases requires the integration of clinical evidence, client preferences, and holistic care principles to ensure client safety and promote positive health outcomes. It also entails educating clients about their medications, monitoring effectiveness, and adjusting treatments as necessary in response to changes in the client’s condition or emerging clinical guidelines. 

Drugs Used to Manage Hypertension

Background

Hypertension affects millions of people around the world and is a primary cause of mortality, potentially leading to the development of cardiovascular disease, renal disease, and stroke. Effective management includes lifestyle changes and medication to reduce blood pressure and prevent complications. With so many drugs available to treat hypertension, nurse practitioners (NPs) must ensure that treatment plans are individualized to specific client circumstances and conditions (Rosenthal & Burchum, 2021). 

Management of Hypertension 
Managing hypertension requires a comprehensive approach to nonpharmacologic interventions and medication therapy using one or more of the below drug classes. Medication selection is influenced by the assessment of an individual’s overall health, comorbidities, and other specific health needs. The choice of medication should be tailored to the individual client, aiming to manage blood pressure and side effects effectively. The following drug classes offer multiple mechanisms to lower blood pressure (Rosenthal & Burchum, 2021).  
Click each section below to learn more about different drug classifications used to manage hypertension. 
Diuretics
Diuretics play a crucial role in managing hypertension by decreasing blood volume through diuresis to contribute to decreased blood pressure. They can be effective when administered alone or with other antihypertensive medications (Rosenthal & Burchum, 2021). 
Click each tab below to learn more about different classifications of diuretics. 
Thiazide Diuretics
Thiazide diuretics target the distal convoluted tubule in the nephron to inhibit sodium and water reabsorption, leading to increased diuresis.
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Overview of the Drug
• Prototype: hydrochlorothiazide (HCTZ) 
• Category: Thiazide diuretic 
• Primary Function: Increases excretion of sodium, chloride, potassium, and water in the distal convoluted tubule. 
• Unique Features: First-line treatment for hypertension. Weaker than loop diuretics. Requires adequate kidney function to work. Promotes calcium reabsorption, which can be helpful for clients with osteoporosis. 
Mechanism of Action
• Thiazide diuretics inhibit sodium and chloride reabsorption in the early distal convoluted tubule in the nephron, causing water to be retained in the nephron rather than reabsorbed and leading to increased diuresis. 
• Since only 10% of the filtered sodium and chloride is normally reabsorbed in the early distal convoluted tubule, the diuretic potential for thiazides is weaker than loop diuretics. 
• Enhances calcium reabsorption in the nephron, beneficial for conditions like postmenopausal osteoporosis. 
Title: Diuretics and the kidney
 
Indications and Therapeutic Uses
• Hypertension: Often the first drug prescribed for a new hypertension diagnosis.
• Heart Failure: Mild to moderate.
• Edema: Less effective than loop diuretics but used for various types of edema. 
• Osteoporosis: Promotes calcium retention. 
Side Effects and Adverse Reactions
Side Effect Description
Hypokalemia An electrolyte imbalance where there is too little potassium. Clients can also experience low magnesium levels.
Hyponatremia An electrolyte imbalance where there is too little sodium. Clients can also experience low chlorine levels.
Hypovolemia Decreased blood volume and dehydration from excessive diuresis. This side effect is less severe than in loop diuretics.
Hypotension Low blood pressure. Orthostatic blood pressure changes can also occur.
Hyperglycemia High blood sugar. Diabetic clients should use caution.
Hyperuricemia High uric acid levels. Clients with gout should use caution.
High cholesterol Elevated LDL levels.
Precautions and Contraindications
Precautions: 
• Requires adequate kidney function for effectiveness. 
• Use with caution in clients with severe electrolyte imbalances. 
• Risks in clients with pre-existing hypotension or at risk for falls. 
• Potential for acute kidney injury in cases of severe dehydration. 
Contraindications:  
• Contraindicated for clients with sulfa allergy. 
• Contraindicated for clients with severe renal impairment. 
Drug Interactions
• Potentiation of other antihypertensive drugs, leading to [hypotension]. 
• The potential for drugs like digoxin and lithium to accumulate and cause toxicity due to [hypokalemia and hyponatremia]. 
• [NSAIDs] can reduce the diuretic effect. 
Dosing, Administration, & Client Teaching 
Dosing
• Dosage varies depending on the condition being treated. 
• Check drug dosing guidelines for individualized dosing. 
• Dosing considerations for clients with different levels of renal function since adequate renal function required. 
• Oral administration, typically once daily. 
Administration
• Oral administration. 
• Consider administration in the morning to avoid nocturia. 
Client Teaching
• Advising clients about potential glucose and uric acid level changes. 
• Importance of monitoring for signs of dehydration and electrolyte imbalance. 
• Daily weights. 
• Advising on the timing of the dose to avoid nocturia (e.g., taking it in the morning). 
• Dietary advice, particularly on potassium-rich foods. 
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
• Blood glucose levels in diabetic clients. 
Serum Drug Levels 
• Serum drug levels for lithium or digoxin, if applicable. 
Uric Acid Levels 
• Monitor uric acid levels for clients with gout or a history of uric acid renal calculi. 
Aldosterone Antagonist (Potassium Sparing) Diuretics 
Aldosterone antagonists, also known as potassium-sparing diuretics, work in the distal nephron to help the body retain potassium while promoting the excretion of sodium and water.
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Overview of the Drug
• Prototypes: Spironalactone (Aldactone) and triamterene (Dyrenium) 
• Category: Potassium-sparing diuretics 
• Spironalactone (Aldactone) is an Aldosterone Antagonist 
• Triamterene (Dyrenium) is a Non-Aldosterone Antagonist 
• Primary Function: Used in combination with other diuretics to mitigate potassium loss, usually in clients who also have heart failure or are post-MI. 
• Unique Features: Scant diuretic effects. Used mainly to offset potassium losses from loop or thiazide diuretics. 
Mechanism of Action
• Spironolactone: Blocks aldosterone receptors in the distal nephron. 
• Triamterene: Directly inhibits the sodium-potassium exchange in the distal nephron (works faster than spironolactone).  
• Both drugs produce only scant diuresis because action occurs late in the nephron, with most fluid already reabsorbed. 
Indications and Therapeutic Uses
• Hypertension: Encourages modest diuresis and counters potassium loss when used with other diuretics to treat hypertension.
• Edema: Encourages modest diuresis and counters potassium loss when used with other diuretics to treat edema.
• Heart Failure: Reduces mortality and hospital readmissions, considered cardioprotective.
Off Label Uses
• Spironalactone is used to manage hormonal acne, hirsutism, or polycystic ovary syndrome (PCOS) due to its anti-androgen effects. 
Side Effects and Adverse Reactions
Side Effect Description
Hyperkalemia An electrolyte imbalance where there is too much potassium. This risk is increased when used with other drugs or salt substitutes that can increase potassium. This side effect can cause cardiac arrhythmias or death.
Delayed onset of action Spironalactone takes up to 48 hours to take effect.
Endocrine effects Due to spironolactone having a structural similarity to steroids, clients can experience gynecomastia, menstrual irregularities, impotence, hirsutism, voice deepening.
Precautions and Black Box Warnings
Precautions
• Caution in clients with high risk of hyperkalemia (renal disease or those who take ACEs, ARBs, salt substitutes (Mrs. Dash), chronic NSAID use, or potassium supplements). 
• Safe handling precautions for pregnant healthcare workers (risk of fetal harm). 
Black Box Warnings
• Hyperkalemia risk associated with renal impairment, diabetes, older adults, and critically ill clients. This could be fatal. 
• Increased tumor risk with spironolactone. 
Drug Interactions
• Enhanced risk of hyperkalemia with medications like [potassium supplements, Angiotensin-converting-enzyme (ACE) inhibitors, Angiotensin receptor blockers (ARBs), and direct renin inhibitors]. 
• Caution with [salt substitutes] high in potassium. 
Dosing, Administration, & Client Teaching 
Dosing
• Dosage varies based on condition and client response. 
• Check drug dosing guidelines for individualized dosing. 
• Oral administration with the delayed effect of spironolactone considered in acute settings. 
• Typically used in long-term management rather than immediate diuresis. 
• Effective in clients with varying kidney functions. 
• Alternative diuretic to thiazides for clients with sulfa allergy.  
• Consider risk vs. benefit in clients with pre-existing conditions that could be exacerbated by hyperkalemia. 
Administration
• Oral administration. 
• Safe handling precautions for pregnant healthcare workers (risk of fetal harm). 
Client Teaching
• Awareness of signs and symptoms of hyperkalemia (e.g., muscle weakness, cardiac irregularities). 
• Importance of regular potassium level monitoring. 
• Advising against the use of potassium-rich salt substitutes. 
• Understanding potential endocrine-related side effects of spironolactone. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
Loop Diuretics
Furosemide (Lasix) is a potent loop diuretic that is effective for clients with varying degrees of kidney function, including those with renal impairment. Loop diuretics work by inhibiting sodium and chloride reabsorption in the nephron’s loop of Henle to produce significant diuresis and subsequent fluid volume reduction. Furosemide can be prescribed for many indications, including edema, heart failure, cirrhosis, kidney disease, pulmonary edema, and hypertension in limited circumstances (for example, if clients do not have adequate renal function and require fluid volume reduction and are hypertensive or clients who have heart failure and hypertension). Due to its mechanism of action, it can result in side effects like electrolyte imbalances and hypovolemia, requiring close monitoring of electrolyte levels and renal function. Loop diuretics are covered later in the lesson when heart failure medications are covered, as that is their primary indication. 
Drugs Suppressing the Renin-Angiotensin-Aldosterone System (RAAS)
The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating fluid volume and blood vessel reactivity to regulate blood pressure; drugs that suppress the RAAS may be used to manage hypertension (Rosenthal & Burchum, 2021). 
Click each tab below to learn more about drugs suppressing the renin-angiotensin-aldosterone system (RAAS). 
ACE Inhibitors
Angiotensin-Converting Enzyme (ACE) inhibitors act on the renin-angiotensin-aldosterone system (RAAS) by preventing the formation of angiotensin II.
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Overview of the Drug
Prototype: captopril (Capoten) 
• Category: ACE Inhibitor  
• Primary Function: Inhibits the conversion of angiotensin I to angiotensin II in the renin-angiotensin-aldosterone system (RAAS), which reduces blood pressure and eases the workload on the heart. 
• Unique Features: Commonly known as ‘prils’ (e.g., captopril, lisinopril, enalapril). 
Mechanism of Action
• ACE inhibitors work by inhibiting the angiotensin-converting enzyme (ACE) normally responsible for converting angiotensin I to angiotensin II in the renin-angiotensin-aldosterone system (RAAS). The reduction in angiotensin II leads to vasodilation, decreased aldosterone secretion, reduced blood volume, and decreased blood pressure. 
• Angiotensin-converting enzyme (ACE) is also called kinase II, depending on its substrate (angiotensin II versus bradykinin). When ACE is inhibited, kinase II is also inhibited. This leads to an accumulation of bradykinin, which also contributes to vasodilation and is responsible for the potential adverse effects of cough and angioedema. 
Title: Renin-Angiotensin-Aldosterone System
1. Na+ deficit Dehydrations
2. Renin
3. Angiotensinogen
4. Angiotensin I (Step circled for this part of the RAAS process.)
5. ACE (Step circled for this part of the RAAS process.)
6. Angiotensin II (Step circled for this part of the RAAS process.)
7. NA+ CL- reabsorption, Vasocostriction, Aldosterone, Posterior Pituitary
Indications and Therapeutic Uses
• Hypertension: The reduction in angiotensin II leads to vasodilation, decreased aldosterone secretion, and reduced blood volume, decreasing blood pressure.
• Heart Failure: Reduces blood pressure and eases the workload on the heart.
• Post MI: Used after a myocardial infarction (MI) to reduce mortality and decrease the incidence of heart failure.
• Stroke and MI Prevention: Used to prevent stroke and MI in clients with cardiovascular risk through reduced vascular resistance.
• Nephropathy: Used in diabetic and nondiabetic nephropathy to slow progression by reducing glomerular filtration pressure.
• Diabetic Retinopathy: Can slow development of retinopathy in type 1 diabetic clients.
Side Effects and Adverse Reactions
Side Effect Description
Hyperkalemia An electrolyte imbalance where there is too much potassium. This risk is increased when used with other drugs or salt substitutes that can increase potassium. This side effect can cause cardiac arrhythmias or death.
First Dose Hypotension After taking an ACE inhibitor for the first time, clients may experience widespread vasodilation and a large drop in blood pressure.
Cough Can occur due to increased bradykinin levels and is generally dry and irritating. This is a reason many clients may stop taking ACE inhibitors.
Renal Failure In clients with renal artery stenosis or only one kidney, ACE inhibitors may cause renal failure.
Angioedema Potentially fatal reaction from increased capillary permeability from elevated bradykinin levels resulting in edema of the tongue, mouth, or face. This can be life-threatening due to airway obstruction.
Neutropenia Rare complication that is more likely in clients with renal impairment and results in decreased neutrophil counts, predisposing clients to infection.
Precautions, Contraindications, & Black Box Warning
Precautions
• Caution in clients also taking other medications reducing blood pressure. 
• Caution in clients taking other medications that raise potassium levels. 
Contraindications 
• Contraindicated in pregnant and breastfeeding clients due to risk of harm. 
• Contraindicated in clients with a history of angioedema related to ACE inhibitors. 
• Contraindicated in clients with renal artery stenosis or one kidney. 
• Contraindicated in clients who develop a dry cough from taking ACE inhibitors. 
Black Box Warning
• Can cause injury and death to the developing fetus in the second and third trimesters of pregnancy. 
Drug Interactions
• Taking [potassium supplements or potassium-sparing diuretics] with ACE inhibitors can increase the risk of hyperkalemia. 
• [NSAIDS] may reduce antihypertensive effects. 
• [Diuretics] and other antihypertensives can increase the risk of hypotension. 
• ACE inhibitors can cause [lithium]toxicity.  
Dosing, Administration, & Client Teaching 
Dosing
• Oral administration, typically once or twice daily.  
• Dosing varies by specific drug and client condition. 
• Check drug dosing guidelines for individualized dosing. 
• Enalapril is available in IV form for acute hypertension management. 
• Dose adjustment may be necessary in renal impairment since ACE inhibitors excreted by the kidneys. Avoid in severe chronic kidney disease (CKD) (eGFR <60). 
• Start dose low to avoid first dose hypotension. 
• New onset of dry cough not accompanied by upper respiratory infection client should switch to an ARB or another antihypertensive drug. 
• Allow 36-hour washout period when switching to DRIs or combination drugs. 
• All except lisinopril are prodrugs. 
• Also available in combination drugs. 
Administration
• Oral administration, typically once or twice daily. 
• Most can be taken with food. 
Client Teaching
• Educate about the importance of adherence and not stopping abruptly. 
• Advise to report any signs of facial swelling, difficulty breathing (angioedema), persistent cough, or significant changes in urine output. 
• Monitor blood pressure regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
• Check kidney function in at-risk populations (older adults, renal artery stenosis, diabetics) 3-5 days after starting the drug. 
Serum Drug Levels
• Serum drug levels for lithium, if applicable. 
Complete Blood Count
• For captopril: Monitor CBC as this is rarely associated with agranulocytosis, neutropenia, and leukopenia. 
Angiotensin II Receptor Blockers
Angiotensin II Receptor Blockers (ARBs) act on the renin-angiotensin-aldosterone system (RAAS) block the actions of angiotensin II at receptor sites throughout the body.
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Overview of the Drug
Prototype: losartan (Cozaar) 
• Category: Angiotensin II receptor blockers (ARBs) 
• Primary Function: Block the action of angiotensin II, resulting in vasodilation, decreased aldosterone secretion, and lower blood pressure. 
• Unique Features: Known as 'sartans' (e.g., losartan, valsartan). 
Mechanism of Action
• Angiotensin II receptor blockers (ARBs) block the action of angiotensin II at the angiotensin II type 1 (AT1) receptors in the kidneys, adrenals, posterior pituitary, and blood vessels. This leads to vasodilation, reduced secretion of vasopressin, and decreased production and release of aldosterone. 
• Because ARBs do not inhibit ACE, there is no increase in bradykinin levels. This reduces the risk of cough and angioedema. 
Title: Renin-Angiotensin-Aldosterone System
1. Na+ deficit Dehydrations
2. Renin
3. Angiotensinogen
4. Angiotensin I 
5. ACE 
6. Angiotensin II 
7. NA+ CL- reabsorption, Vasocostriction, Aldosterone, Posterior Pituitary (Step circled for this part of the RAAS process.)
Indications and Therapeutic Uses
• Hypertension: The reduction in angiotensin II action leads to vasodilation, decreased aldosterone secretion, and reduced blood volume, decreasing blood pressure.
• Heart Failure: Used as an alternative to ACE inhibitors, particularly in clients intolerant to ACE inhibitors.
• Nephropathy: Used in diabetic nephropathy to slow progression by reducing glomerular filtration pressure.
• Post MI: Used after a myocardial infarction (MI) to reduce mortality and decrease the incidence of heart failure.
• Stroke and MI Prevention: Used to prevent stroke and MI in clients with cardiovascular risk through reduced vascular resistance.
• Diabetic Retinopathy: Can slow development of retinopathy in type 1 diabetic clients.  
Side Effects and Adverse Reactions
Side Effect Description
Hyperkalemia An electrolyte imbalance where there is too much potassium. This risk is increased when used with other drugs or salt substitutes that can increase potassium. This side effect can cause cardiac arrhythmias or death.
Renal Failure In clients with renal artery stenosis or only one kidney, ARBs can cause this.
Angioedema Potentially fatal reaction from increased capillary permeability and edema of the tongue, mouth, or face. This can be life-threatening due to airway obstruction. Lower risk than in ACE inhibitors.
Precautions, Contraindications, and Black Box Warning
Precautions
• Caution in clients also taking other medications reducing blood pressure. 
• Caution in clients taking other medications that raise potassium levels. 
Contraindications
• Contraindicated in pregnant and breastfeeding clients due to risk of harm. 
• Contraindicated in clients with renal artery stenosis or one kidney. 
Black Box Warning
• Can cause injury and death to the developing fetus in the second and third trimesters of pregnancy. 
Drug Interactions
• Taking [potassium supplements or potassium-sparing diuretics] with ARBs can increase the risk of hyperkalemia. 
• [Diuretics] and other antihypertensives can increase the risk of hypotension. 
Dosing, Administration, & Client Teaching 
Dosing
• Oral administration, with dosing varying by specific drug and condition. 
• Often started at a low dose and adjusted based on response and tolerability. 
• Check drug dosing guidelines for individualized dosing. 
• Allow 36-hour washout period when switching to direct renin inhibitors (DRIs) or combination drugs. 
• Avoid in severe CKD (eGFR <60). 
• Also available in combination drugs. 
Administration
• Oral administration. 
• May be taken with or without food. 
Client Teaching
• Pregnant clients or those planning to become pregnant should discuss medication risks and alternatives. 
• Importance of medication adherence and regular monitoring of blood pressure. 
• Awareness of potential side effects like dizziness and changes in renal function. 
Labs to Monitor 
Basic Metabolic Panel (BMP)
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
• Check kidney function in at-risk populations (older adults, renal artery stenosis, diabetics) 3-5 days after starting the drug. 
Direct Renin Inhibitors 
Direct Renin Inhibitors (DRIs) are a class of antihypertensive drugs that specifically target and inhibit the activity of renin, the enzyme responsible for initiating the renin-angiotensin-aldosterone system (RAAS). By inhibiting renin, DRIs effectively reduce the conversion of angiotensinogen to angiotensin I, which in turn leads to lower levels of angiotensin II, a potent vasoconstrictor. This results in vasodilation and a subsequent decrease in blood pressure. Aliskiren (Tekturna) is the prototypical drug in this category and is only used for the treatment of hypertension. It is particularly beneficial in clients who have not achieved blood pressure control with other antihypertensives. DRIs are generally well-tolerated but should be used cautiously in certain populations, including clients with renal impairment. They also have the potential for interaction with other medications affecting the RAAS and are contraindicated during pregnancy due to the risk of fetal harm. Regular monitoring of kidney function and potassium levels is recommended for clients on DRIs (Rosenthal & Burchum, 2021). 

Renin-Angiotensin-Aldosterone System Image Description 
Title: Renin-Angiotensin-Aldosterone System
1. Na+ deficit Dehydrations
2. Renin (Step circled for this part of the RAAS process.)
3. Angiotensinogen
4. Angiotensin I
5. ACE
6. Angiotensin II
7. NA+ CL- reabsorption, Vasocostriction, Aldosterone, Posterior Pituitary
Learn By Applying
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Learn By Applying Transcript
Which of the following are potential side effects of taking ACE Inhibitors? Select all that apply. 
• Cough (Correct answer)
• Angioedema (Correct answer)
• Digoxin toxicity 
• First dose hypotension (Correct answer)
• Hypokalemia 
• Hyperkalemia (Correct answer)
Rationale: ACE inhibitors can cause cough, angioedema, first dose hypotension, and hyperkalemia. Hypokalemia and digoxin toxicity (usually precipitated by hypokalemia) are not potential side effects. 
Calcium Channel Blockers
Calcium channel blockers relax blood vessels by inhibiting calcium from entering cardiac and/or arterial muscle cells, depending on their classification as dihydropyridines (working only on the vascular smooth muscle) or non-dihydropyridines (working on cardiac and arterial muscle cells).
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Overview of the Drug
Prototypes: nifedipine (Procardia) and verapamil (Calan) 
• Category: Calcium Channel Blockers 
• Nifedipine (Procardia) and amlodipine (Norvasc) are Dihydropyridine(affecting blood vessels) 
• Verapamil (Calan) and diltiazem (Cardizem) are Non-dihydropyridine(affect the heart and blood vessels) 
• Primary Function: They inhibit the influx of calcium ions into myocardial and vascular smooth muscle cells, causing vasodilation and reducing cardiac workload. 
• Unique Features: Two types of calcium channel blockers: dihydropyridines that affect blood vessels and non-dihydropyridines that affect the heart and blood vessels. 
Mechanism of Action
Dihydropyridines Non-Dihydropyridines
• Dihydropyridines mainly dilate peripheral arterioles, reducing systemic vascular resistance and arterial pressure. This reduces afterload and therefore cardiac workload and myocardial oxygen demand. • Non-dihydropyridines bind calcium channels in the heart and blood vessels. This reduces afterload and cardiac workload, decreasing myocardial oxygen demands.
◦ Heart: Binding calcium channels in cardiac myocytes and nodal tissue (SA and AV nodes) causes decreased contractility, decreased heart rate, and decreased conductivity
◦ Blood Vessels: Binding calcium channels causes vasodilation.
Indications and Therapeutic Uses
• Hypertension: Dilation of arterioles contributes to a reduction in blood pressure.
• Angina: Arteriole dilation reduces afterload and therefore decreases myocardial oxygen demand. They also relax coronary vasospasm, useful in variant (Printzmetal) angina.
• Arrhythmias: Suppressing conduction through the AV node can reduce the incidence of supraventricular tachycardias (atrial fibrillation, atrial flutter, and SVT).
Side Effects and Adverse Reactions
Side Effect Description
Constipation This side effect happens from blocking calcium channels in intestinal smooth muscle and is more common in older adults taking non-dihydropyridines. This can be minimized by increasing dietary fiber and fluids.
Headache, flushing, peripheral edema, dizziness Can occur from vasodilation.
Bradycardia, atrioventricular (AV) block Non-dihydropyridines can compromise cardiac function in clients with certain cardiac dysfunction.
Reflex tachycardia In dihydropyridines this can happen due to reflex increase in sympathetic activity related to a fast drop in cardiac output from vasodilation.
Precautions and Contraindications
Precautions
• Grapefruit juice can inhibit metabolism of many calcium channel blockers and potentially cause toxicity. 
• Use non-dihydropyridines cautiously in clients with heart failure. Clients with systolic heart failure (heart failure with reduced ejection fraction; HRrEF) can experience worsening heart failure due to decreased contractility. 
• Caution in elderly clients due to increased sensitivity and risk of side effects. 
• Dose adjustment may be necessary in clients with severe hepatic impairment. 
Contraindications
• Avoid non-dihydropyridines in clients with AV block, bradycardia, and heart failure with reduced ejection fraction. 
• Avoid in clients with severe hypotension or cardiogenic shock. 
• Pregnancy category C: Weigh risks and benefits in pregnant and breastfeeding clients. 
Drug Interactions
• [Beta-blockers and Digoxin] can increase the risk of bradycardia and AV block, especially when used with non-dihydropyridines. 
• [Grapefruit juice] consumption can increase levels of certain calcium channel blockers, leading to toxicity. 
Dosing, Administration, & Client Teaching 
Dosing
• Oral administration, with doses varying depending on the specific drug and condition being treated. 
• Check drug dosing guidelines for individualized dosing. 
• Dose adjustment may be necessary in hepatic impairment. 
• Avoid non-dihydropyridines in clients with HFrEF due to their effects on contractility. 
• Formulations can be immediate release or extended-release for once-daily dosing. 
• Initiation at lower doses with gradual titration to minimize side effects. 
• Order calcium channel blockers and other cardiosuppressive drugs (e.g., digoxin, beta-blockers, etc.) several hours apart. 
Administration
• Oral administration. 
• Avoid grapefruit juice. 
• Administer calcium channel blockers and other cardiosuppressive drugs (e.g., digoxin, beta-blockers, etc.) several hours apart. 
Client Teaching
• Educate about potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and regular monitoring of blood pressure and heart rate. 
• Emphasize the avoidance of grapefruit juice while taking certain CCBs. 
• Advise clients to report symptoms like significant swelling, severe dizziness, or palpitations. 
• Monitor for signs of heart failure, especially in clients with pre-existing heart conditions. 
Labs to Monitor 
Liver Function Tests (LFTs) 
• Regular liver function tests may be required for certain clients. 
Learn By Applying
Apply what you have learned to the question below. 
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Learn By Applying Transcript
The NP is seeing a client with hypertension and heart failure with reduced ejection fraction (HFrEF). Which calcium channel blocker would be most appropriate for this client?  
• Nifedipine (Procardia), a dihydropyridine (Correct answer)
• Verapamil (Calan), a non-dihydropyridine 
Rationale: Nifedipine (Procardia), a dihydropyridine, would be most appropriate for this client with HFrEF. Dihydropyridines mostly affect the blood vessels, promoting vasodilation to reduce blood pressure. Non-dihydropyridines also affect the heart, causing decreased heart rate, contractility, and conductivity. This reduction in contractility could further compromise the cardiovascular status of clients with HFrEF and should, therefore, be avoided. 
Drugs Interacting with Sympathetic Nervous System (SNS) Receptors
Drugs that interact with the sympathetic nervous system (as antagonists or, in the case of alpha-2, agonists) can influence many physiologic processes through interactions with the heart, blood vessels, and other structures. Those effects can help providers manage hypertension (Rosenthal & Burchum, 2021). 
Click each tab below to learn more about drugs interacting with sympathetic nervous system (SNS) receptors. 
Alpha-Blockers
Alpha-blockers block sympathetic alpha-1 receptors to relax smooth muscle in the blood vessels, prostate, and bladder neck muscles.
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Overview of the Drug
Prototype: prazosin (Minipress) 
• Category: Alpha-1 Adrenergic Blocking Agent 
• Primary Function: Block alpha-1 adrenergic receptors in the blood vessels and prostate and bladder neck muscles to treat hypertension and/or BPH. 
• Unique Features: Many drugs in this category end in -osin. 
Mechanism of Action
• Alpha 1 adrenergic blockers selectively block alpha-1 adrenergic receptors to inhibit the action of norepinephrine in the blood vessels and smooth muscles of the bladder neck and prostate. The result is vasodilation of arteries and veins to lower blood pressure. It can also be used to treat clients with BPH. 
• Some alpha-1 blockers are only used to treat BPH while some treat hypertension and BPH.  
Normal Action of Agonists in Adrenergic Receptors Action When Alpha-1 is Blocked
• Alpha-1: When alpha-1 is filled with agonist, blood vessels vasoconstrict to increase blood pressure. Additionally, the prostate and bladder neck contract and pupils dilate.
• Alpha-2: Alpha-2 receptors are centrally acting and normally release norepinephrine to fill their own receptor, resulting in decreased sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation.
• Beta-1: Filling beta-1 receptors in the heart increases heart rate, conductivity, and contractility.
• Beta-2: Filling beta-2 receptors in the lungs causes bronchodilation and glycogenesis (the breakdown of glycogen to release glucose into the bloodstream for energy). • Blocking alpha-1 results in vasodilation, relaxation of the prostate and bladder neck, and constricted pupils.
Indications and Therapeutic Uses
• Hypertension: Lowers blood pressure through vasodilation.
• BPH: Eases urinary symptoms from benign prostatic hypertrophy (BPH) by relaxing bladder and prostate muscles.
• Pheochromocytoma: Blocks the action of excessive catecholamine release and subsequent hypertension associated with pheochromocytoma.
• Alpha-1 Agonist Reversal: Can be used to reverse local and systemic vasoconstriction from alpha-adrenergic agonists like epinephrine.
• Raynaud’s Phenomenon: Reduces the frequency and severity of attacks through preventing vasoconstriction.
Side Effects and Adverse Reactions
Side Effect Description
Reflex tachycardia This can happen due to reflex increase in sympathetic activity related to a fast drop in cardiac output from vasodilation.
Orthostatic Hypotension Sudden drop in blood pressure upon standing. This can cause dizziness or syncope.
Nasal Congestion This can happen from vasodilation in nasal blood vessels.
Inhibition of Ejaculation This can happen due to blockade of alpha-1 receptors required for sexual function.
Increased Blood Volume Reducing blood pressure can lead to activation of the RAAS process, resulting in this.
Precautions
Precautions
• Risk of severe hypotension, including orthostatic hypotension. 
• Risk for excessive blood pressure reduction when taken with other antihypertensive medications. 
• Elderly clients have a higher susceptibility to side effects like dizziness and falls. 
• Phosphodiesterase inhibitors can cause unsafe reductions in blood pressure when taken with alpha-1 blockers. 
Drug Interactions
• When taken with other [antihypertensive agents] there could be an excessive reduction in blood pressure. 
• When taken with agents for erectile dysfunction, such as [phosphodiesterase inhibitors], there can be severe hypotension. 
Dosing, Administration, & Client Teaching 
Dosing
• Check drug dosing guidelines for individualized dosing. 
• Initial low dose recommended to minimize first-dose effect (significant drop in blood pressure). 
• Usually ordered orally, once or twice daily. 
• Monitor liver function tests for specific drugs in this category. 
Administration
• Typically administered orally, once or twice daily. 
• Assess heart rate and blood pressure prior to administration. 
Client Teaching
• Educate the client to take at bedtime to avoid hypotension and falls. 
• Be aware of first dose hypotension and have someone with them to avoid injury. 
• Educate about potential blood pressure changes and risk of dizziness or falls. This should include taking precautions while driving. 
• Educate about the importance of adherence and regular monitoring of blood pressure and heart rate. 
• Caution about standing up quickly to avoid dizziness and falls. 
• Awareness of possible side effects like nasal congestion and sexual dysfunction. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Monitor renal function (BUN and creatinine) especially in clients with pre-existing kidney conditions. 
Liver Function Tests (LFTs) 
• Regular liver function tests may be required for certain clients. 
Beta-Blockers
Beta-blockers block sympathetic beta receptors, influencing heart rate, heart rhythm, contractility, cardiac oxygen demand, and cardiac output, with potential effects on the respiratory system and glucose regulation as well depending on the receptor selectivity of the medication.
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Overview of the Drug
Prototypes: propranolol (Inderal) and metoprolol (Lopressor) 
• Category: Beta-blockers 
• Propranolol (Inderal) is a Nonselective Beta-blocker(affecting beta-1 and beta-2 adrenergic receptors and therefore the heart and lungs) 
• Metoprolol (Lopressor) is a Selective Beta-blocker (affect only beta-1 adrenergic receptor and therefore only the heart) 
• Primary Function: Block beta-1 adrenergic receptors in the heart to decrease heart rate, contractility, and conductivity to create an overall reduction in cardiac output and therefore blood pressure. 
• Unique Features: Subdivided into non-selective (beta-1 and beta-2) and selective (beta-1) blockers. All drugs in this class end in -olol. 
Mechanism of Action
• Non-Selective Beta Blockers: Block beta adrenergic receptors in the heart (beta-1) and the lungs (beta-2), leading to reduced heart rate, conductivity, and contractility and bronchoconstriction. 
• Selective Beta-1 Blockers: Block beta adrenergic receptors in the heart, reducing heart rate, force of contraction, and conduction velocity. These are beneficial to clients who could experience adverse health outcomes from beta-2 blockade (e.g., bronchoconstriction and hypoglycemia). 
Normal Action of Agonists in Adrenergic Receptors Action When Beta Receptors are Blocked
• Alpha-1: When alpha-1 is filled with agonist, blood vessels vasoconstrict to increase blood pressure. Additionally, the prostate and bladder neck contract and pupils dilate.
• Alpha-2: Alpha-2 receptors are centrally acting and normally release norepinephrine to fill their own receptor, resulting in decreased sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation.
• Beta-1: Filling beta-1 receptors in the heart increases heart rate, conductivity, and contractility.
• Beta-2: Filling beta-2 receptors in the lungs causes bronchodilation and glycogenesis (the breakdown of glycogen to release glucose into the bloodstream for energy). • Blocking beta-1 adrenergic receptors in the heart leads to reduced heart rate, conductivity, and contractility.
• Blocking beta-2 receptors in the lungs leads to bronchoconstriction and the inhibition of glycogenolysis.
Indications and Therapeutic Uses
• Hypertension: Blocking beta-1 adrenergic receptors in the heart decreases heart rate, contractility, and conductivity to create an overall reduction in cardiac output and, therefore, blood pressure.
• Angina: Blocking beta-1 adrenergic receptors in the heart decreases heart rate, contractility, and conductivity to decrease myocardial workload and, therefore, oxygen demand. 
• Arrhythmias: Blocking beta-1 adrenergic receptors in the heart decreases heart rate and conductivity through the SA and AV nodes to manage arrhythmias.
• Post MI: Reduces mortality and risk of subsequent MI due to reduction in cardiac oxygen demand from slowed heart rate and decreased contractility.
• Heart Failure: Some beta-blockers can be effective in improving morbidity by reducing myocardial workload for clients with some types of heart failure.
• Hyperthyroidism: Beta-blockers can control some symptoms of hyperthyroidism, such as tachycardia.
• Migraine Prophylaxis: Beta-blockers can reduce the frequency and severity of migraines (not indicated for acute treatment).
• Performance Anxiety: Beta-blockers can treat performance anxiety symptoms, including tachycardia, tremors, and sweating from SNS activation (“fight or flight”). 
• Pheochromocytoma: Blocks the action of excessive catecholamine release and subsequent tachycardia associated with pheochromocytoma.
• Glaucoma: Topical beta-blockers can reduce intraocular pressure. 
Side Effects and Adverse Reactions
Side Effect Description
Rebound Cardiac Excitation Abrupt withdrawal of beta-blockers can cause tachycardia and ventricular arrhythmias.
Reduced Cardiac Output Decreased heart rate, contractility, and conductivity could reduce this and precipitate or worsen heart failure.
Bradycardia, AV block Beta-blockers can compromise cardiac function in clients with certain cardiac dysfunction related to heart rate and rhythm. This could also cause hypotension.
Worsening Respiratory Status Non-selective beta blockers also block beta-2 receptors in the lungs, potentially causing bronchoconstriction. This means non-selective beta blockers (propranolol) are not indicated for clients with certain respiratory conditions.
Masking Hypoglycemia Normally, hypoglycemia causes an increase in heart rate. Blocking beta-1 receptors in the heart can block this tachycardic response and therefore cause this.
Hypoglycemia Normally, filling beta-2 receptors causes glycogenolysis. Blocking this with non-selective beta-blockers causes this alteration in blood sugar, which can be problematic for diabetic clients.
CNS reactions Beta-blockers cross the blood-brain barrier, rarely causing depression, insomnia, nightmares, or hallucinations.
Neonatal Symptoms Taking beta-blockers in pregnancy can predispose newborns to bradycardia, respiratory distress, and hypoglycemia since these drugs cross the placenta.
Precautions, Contraindications, and Black Box Warning
Precautions
• Use cautiously in clients with depression since beta-blockers can cross the blood-brain barrier. 
• Monitor neonates of clients taking beta-blockers carefully for bradycardia, respiratory distress, and hypoglycemia. 
• Use caution with selective beta-blockers in diabetic clients due to beta-1 blockade that masks hypoglycemia symptoms (non-selective beta-blockers are contraindicated in diabetic clients). 
• Ensure the drug is not abruptly discontinued to prevent rebound cardiac excitation. 
• Use cautiously in heart failure. In HFrEF, beta blockers can worsen symptoms. 
Contraindications
• Contraindicated in clients with severe anaphylactic reactions that rely on epinephrine during anaphylaxis. Blocking beta receptors could prevent those sites from being filled with epinephrine when needed for anaphylaxis rescue use. 
• Contraindicated in clients with bradycardia and heart block. 
• Non-selective beta-blockers are contraindicated in clients with diabetes. 
• Non-selective beta-blockers are contraindicated in clients with respiratory conditions like asthma, COPD, emphysema, and chronic bronchitis. 
Black Box Warning
• For sotalol (Betapace), clients must be monitored using ECG for three days and creatinine clearance must be checked before initiating. 
• For atenolol, metoprolol, nadolol, and timolol, abrupt discontinuation can cause angina or MI. 
Drug Interactions
• Taking beta-blockers with other antihypertensive drugs, especially [calcium channel blockers], can cause excessive cardiosuppression. 
• Taking [insulin] along with non-selective beta-blockers can cause hypoglycemia due to the ability of non-selective beta-blockers to prevent glycogenolysis to correct hypoglycemia. 
• Beta-blockers should be avoided in clients with a history of [anaphylaxis] because they block the effect of drugs like [epinephrine].  
Dosing, Administration, & Client Teaching 
Dosing
• Dosage varies by indication and client response. 
• Check drug dosing guidelines for individualized dosing. 
• Oral, IV, and topical formulations available. 
• Gradual dosage adjustment recommended. 
• Non-selective beta-blockers are not indicated for clients with respiratory conditions or diabetes. 
Administration
• Oral administration is common and IV administration is available in acute settings. Topical administration is used to manage conditions like glaucoma. 
• Assess heart rate and blood pressure prior to administration. 
Client Teaching
• Importance of compliance and gradual withdrawal to avoid rebound cardiac excitation. 
• Monitor blood pressure and heart rate regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Monitoring for side effects including bradycardia, dizziness, breathing difficulties, or hypoglycemia. 
• Diabetic clients should regularly monitor blood sugar due to hypoglycemia masking. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Monitor blood glucose levels for diabetic clients (using BMP or POC glucose). 
Combined Alpha and Beta-Blockers
Combined alpha and beta-blockers block sympathetic alpha and beta receptors, leading to vasodilation and reduced heart rate, contractility, and conductivity.
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Overview of the Drug
Prototype: carvedilol (Coreg) 
• Category: Combined Alpha and Beta-Blocker 
• Primary Function: Simultaneously block alpha-1 and beta-adrenergic receptors, leading to vasodilation and reduced heart rate, contractility, and conductivity. 
• Unique Features: Unique in their dual action affecting vascular tone and cardiac function. 
Mechanism of Action
• Carvedilol blocks alpha-1 adrenergic receptors and beta-1 and beta-2 receptors. 
• Alpha-1 blockade leads to vasodilation, reducing peripheral vascular resistance and lowering blood pressure. 
• Beta blockade (both beta-1 and beta-2) decreases heart rate, myocardial contractility, and reduces renin release from the kidneys. Since it also blocks beta-2, caution should be used in clients with respiratory conditions and diabetes. 
 
Normal Action of Agonists in Adrenergic Receptors Action When Alpha-1 and Beta Receptors are Blocked
• Alpha-1: When alpha-1 is filled with agonist, blood vessels vasoconstrict to increase blood pressure. Additionally, the prostate and bladder neck contract and pupils dilate.
• Alpha-2: Alpha-2 receptors are centrally acting and normally release norepinephrine to fill their own receptor, resulting in decreased sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation.
• Beta-1: Filling beta-1 receptors in the heart increases heart rate, conductivity, and contractility.
• Beta-2: Filling beta-2 receptors in the lungs causes bronchodilation and glycogenesis (the breakdown of glycogen to release glucose into the bloodstream for energy). • Blocking alpha-1 receptors results in vasodilation, relaxation of the prostate and bladder neck, and constricted pupils.
• Blocking beta-1 adrenergic receptors in the heart leads to reduced heart rate, conductivity, and contractility.
• Blocking beta-2 receptors in the lungs leads to bronchoconstriction and the inhibition of glycogenolysis.
Indications and Therapeutic Uses
• Hypertension: Blocking beta-1 adrenergic receptors in the heart decreases heart rate, contractility, and conductivity to create an overall reduction in cardiac output. Combining those effects with the vasodilation produced from blocking alpha-1 adrenergic receptors helps reduced blood pressure and cardiac workload.
• Post MI: Reduces mortality and risk of subsequent MI due to reduction in cardiac oxygen demand from slowed heart rate, decreased contractility, and decreased afterload.
• Heart Failure: These drugs can be effective in improving morbidity by reducing myocardial workload for clients with some types of heart failure.
Side Effects and Adverse Reactions
Side Effect Description
Orthostatic Hypotension Sudden drop in blood pressure upon standing. This can cause dizziness or syncope.
Bradycardia, AV block These drugs can compromise cardiac function in clients with certain cardiac dysfunction related to heart rate and rhythm. This could also cause hypotension.
Worsening Respiratory Status These drugs also block beta-2 receptors in the lungs, potentially causing bronchoconstriction. This means they are not indicated for clients with certain respiratory conditions.
Masking Hypoglycemia Normally, hypoglycemia causes an increase in heart rate. Blocking beta-1 receptors in the heart can block this tachycardic response and therefore cause this.
Hypoglycemia Normally, filling beta-2 receptors causes glycogenolysis. Blocking this causes this alteration in blood sugar, which can be problematic for diabetic clients.
Precautions and Contraindications
Precautions
• Use cautiously in heart failure. In HFrEF, these drugs can worsen symptoms. 
• Caution required in gradual withdrawal to avoid rebound hypertension or angina. 
• Risk of severe hypotension, including orthostatic hypotension. 
• Risk for excessive blood pressure reduction when taken with other antihypertensive medications. 
• Elderly clients have a higher susceptibility to side effects like dizziness and falls. 
• Phosphodiesterase inhibitors can cause unsafe reductions in blood pressure when taken with alpha-1 blockers. 
Contraindications 
• Contraindicated in clients with severe anaphylactic reactions that rely on epinephrine during anaphylaxis. Blocking beta receptors could prevent those sites from being filled with epinephrine when needed for anaphylaxis rescue use. 
• Contraindicated in clients with bradycardia and heart block. 
• Contraindicated in clients with diabetes. 
• Contraindicated in clients with respiratory conditions like asthma, COPD, emphysema, and chronic bronchitis. 
Drug Interactions
• These drugs can interact with other [antihypertensive drugs], potentially causing hypotension or excessive cardiosuppression. 
• Other drugs that decrease blood sugar, including [insulin and oral hypoglycemic agents], can increase the risk of hypoglycemia. 
• When taken with agents for erectile dysfunction, such as [phosphodiesterase inhibitors], there can be severe hypotension. 
• These drugs should be avoided in clients with a history of [anaphylaxis] because they block the effect of drugs like [epinephrine]. 
Dosing, Administration, & Client Teaching 
Dosing
• Check drug dosing guidelines for individualized dosing. 
• Start dose low to avoid first dose hypotension. 
• Oral administration, with dosage tailored to client response and tolerance. 
• Not indicated for clients with respiratory conditions or diabetes. 
• Helpful for countering reflex tachycardia that can occur from isolated alpha-blocking. 
Administration
• Oral administration. 
• Assess heart rate and blood pressure prior to administration. 
Client Teaching
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Monitor blood pressure and heart rate regularly, especially after initiating therapy. 
• Advise clients about potential respiratory and blood sugar symptoms. 
Labs to Monitor 
Basic Metabolic Panel (BMP) 
• Monitor blood glucose as blocking beta-2 can cause hypoglycemia. 
Alpha-2 Receptor Agonists
Alpha-2 receptor agonists stimulate alpha-2 receptors in the central nervous system (CNS) to reduce sympathetic outflow from the central nervous system to exert an effect on the heart and blood vessels.
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Overview of the Drug
Prototype: clonidine (Catapres) 
• Category: Centrally Acting Alpha-2 Agonist 
• Primary Function: Act centrally on alpha-2 adrenergic receptors in the brain to decrease sympathetic outflow, leading to reduced blood pressure. 
• Unique Features: Sympathetic agonist that lowers blood pressure due to unique activity of alpha-2 receptors in the brain where norepinephrine fills its own receptor. 
Mechanism of Action
• Alpha-2 receptor agonists stimulate alpha-2 receptors in the central nervous system in an area of the brainstem that regulates cardiac function. This inhibits the release of norepinephrine, decreasing sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation. 
Normal Action of Agonists in Adrenergic Receptors Action When Alpha-2 is Filled
• Alpha-1: When alpha-1 is filled with agonist, blood vessels vasoconstrict to increase blood pressure. Additionally, the prostate and bladder neck contract and pupils dilate.
• Alpha-2: Alpha-2 receptors are centrally acting and normally release norepinephrine to fill their own receptor, resulting in decreased sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation.
• Beta-1: Filling beta-1 receptors in the heart increases heart rate, conductivity, and contractility.
• Beta-2: Filling beta-2 receptors in the lungs causes bronchodilation and glycogenesis (the breakdown of glycogen to release glucose into the bloodstream for energy). • Alpha-2 receptor agonists stimulate alpha-2 receptors in the central nervous system in an area of the brainstem that regulates cardiac function. This inhibits the release of norepinephrine, decreasing sympathetic tone and results in decreased heart rate, reduced cardiac output, and vasodilation.
Indications and Therapeutic Uses
• Hypertension: The decreased cardiac output and vasodilation of alpha-2 agonists are effective in treating hypertension.
• Pain: Alpha-2 receptor agonists can be used to treat pain, particularly neuropathic pain.
• ADHD: Can be used to treat Attention-Deficit Hyperactivity Disorder (ADHD), particularly in cases where stimulant medications are not suitable. 
Off-Label Uses
Alpha-2 agonists can be used off-label for: 
• Smoking cessation. 
• Treating oppositional defiant disorder and Tourette syndrome. 
• Mitigating symptoms of opioid or nicotine withdrawal. 
Side Effects and Adverse Reactions
Side Effect Description
Sedation and Drowsiness This can occur from CNS affects and is common. Clients should avoid hazardous activities if they are not alert during the first few weeks of treatment.
Xerostomia (a.k.a. dry mouth) A common reaction but irritating to clients and causes medication noncompliance, although not dangerous.
Rebound Hypertension Occurs if medication is abruptly discontinued.
Euphoria At high doses, clonidine can cause this as well as hallucinations, which some clients may be seeking. This can lead to abuse.
Bradycardia and Hypotension From reduced sympathetic activity, these symptoms can occur.
CNS Symptoms Including vivid dreams, nightmares, anxiety, or depression.
Constipation Hazardous in clients with decreased bowel motility and older adults.
Precautions and Contraindications
Precautions
• Caution with clients with a history of substance abuse. 
• Gradual tapering is necessary to avoid rebound hypertension upon discontinuation. 
• Caution in clients with cerebral vascular disease or recent stroke. 
Contraindications
• Contraindicated in pregnancy due to embryotoxic studies in animals. Rule out pregnancy before prescribing. 
• Not recommended in clients with a history of bradycardia or AV block. 
Drug Interactions
• Alpha-2 agonists may interact with other CNS depressants, such as[benzodiazepines], alcohol, or opioids], leading to excessive sedation. 
• Using alpha-2 agonists with other[antihypertensive drugs] may result in hypotension. 
Dosing, Administration, & Client Teaching 
Dosing
• Check drug dosing guidelines for individualized dosing. 
• Oral and transdermal formulations available. 
• Initial dosing should be low, gradually titrated to minimize side effects. 
• Rule out pregnancy before prescribing. 
• Very lipid soluble and acts quickly. 
Administration
• Oral or transdermal administration. 
• Wear gloves when administering transdermal patches. 
• Assess heart rate and blood pressure prior to administration. 
Client Teaching
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Advise clients about the risk of sedation and the need to avoid operating heavy machinery. 
• Monitor blood pressure regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Encouragement to report any signs of depression or significant changes in mood. 
• Instruct on the proper use of transdermal patches. 
• Avoid dry mouth with candies, gum, water. 
Labs to Monitor 
Basic Metabolic Panel (BMP)
• Monitor BUN and creatinine as alpha-2 agonists are renally excreted. This is especially true in elderly clients or those with known renal impairment. 
Liver Function Tests (LFTs)
• Monitor liver function tests (LFTs) as alpha-2 agonists are metabolized with the liver. 
Learn By Applying
Apply what you have learned to the questions below. 
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Quesiton 1
Blocking alpha 1 receptors causes vasodilation and lowers blood pressure. Lowering blood pressure too quickly sends a signal to baroreceptors to maintain cardiac output by increasing heart rate, called ___________. 
Correct answer: Reflex tachycardia 
Rationale: When blood pressure drops too quickly, baroreceptors sense the reduction in cardiac output and increase sympathetic activity, resulting in reflex tachycardia.  
 
Question 2
Which of the following clients may experience difficulty taking nonselective beta-blockers? Select all that apply. 
• Asthma (Correct answer)
• COPD (Correct answer)
• Hypertension 
• Diabetes (Correct answer)
Rationale: Clients with respiratory conditions, such as asthma and COPD, should not take non-selective beta-blockers. Non-selective beta-blockers can cause bronchoconstriction due to their blockade of beta-2 receptors in the lungs. Diabetic clients also should not take non-selective beta-blockers. Non-selective beta-blockers also inhibit glycogenolysis through their blockade of beta-2, potentially causing hypoglycemia. 
Direct-Acting Vasodilators
Direct-acting vasodilators like hydralazine (Apresoline) and nitroprusside (Nipride) are in a class of powerful antihypertensive drugs that directly relax vascular smooth muscle, leading to vasodilation and a subsequent decrease in blood pressure. Hydralazine selectively vasodilates arterioles (decreasing afterload) while nitroprusside relaxes arterioles and veins (impacting afterload and preload). These medications are particularly effective in managing severe hypertension and hypertensive emergencies.  
Hydralazine is often used in chronic management of hypertension in PO form, especially in clients with heart failure, while the IV form is reserved for hypertension management in acute settings. Nitroprusside is typically reserved for acute hypertensive crises due to its potent and rapid-acting effects and is given via IV titration in critical care settings. It is crucial to monitor clients receiving these medications closely for potential adverse effects, including reflex tachycardia, hypotension, renin release, and fluid retention. To mitigate these effects, these drugs can be used in combination with a beta blocker and a diuretic. Hydralazine can also lead to a rare but serious side effect resembling systemic lupus erythematosus (SLE) and is therefore considered a third-line treatment for chronic hypertension. Additionally, these medications may interact with other antihypertensives, enhancing their hypotensive effect (Rosenthal & Burchum, 2021). 
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Lifespan Considerations 
Click each plus (+) sign in the activity below to learn more about lifespan considerations for pharmacologic management of hypertension (Rosenthal & Burchum, 2021). 
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Pregnant and Breastfeeding Clients
• In 2015, the FDA revised pregnancy labeling guidelines to move away from the A, B, C, D, and X labels to the Pregnancy and Lactation Labeling Rule (PLLR), which requires labels to a summary of the risk of using the drug during pregnancy and lactation, data supporting the summary, and counseling information. These labels must be updated when new information is available. Although the PLLR is recommended, original labeling categories are often referenced in practice and across settings and, therefore, provided in this course.Consider the safety of antihypertensive drugs for pregnant and breastfeeding clients. 
• What pregnancy category is the drug? 
• Highly lipid-soluble drugs cross membranes and may enter breastmilk. 
• Drastic reductions in blood pressure may impact perfusion to the placenta in pregnant clients.  
• Hypertension treatment in pregnancy may not be needed after delivery. 
• Consider altered pharmacokinetics related to pregnancy. 
Pediatric Clients
• Consider primary versus secondary hypertension. 
• Secondary hypertension has an identifiable cause and is a more common cause of hypertension in pediatric clients and requires treatment of the underlying cause. 
• Consider the ability of the family to manage a medication regimen. 
• Consider altered pharmacokinetics based on age. 
Older Adults
• Consider the risk for orthostatic hypotension, dizziness, and falls in older adults. 
• Consider the ability of the client and support system to safely self-administer medications without skipping or doubling doses. 
• Consider how dietary patterns may alter electrolytes and compound the effects of some drugs.  
• Consider altered pharmacokinetics based on age-related changes. 
• Consider polypharmacy and drug interactions. 

Clinical Practice Guidelines for Hypertension 
Clinical practice guidelines (CPGs) for hypertension outline evidence-based recommendations for diagnosing and managing high blood pressure, incorporating lifestyle modifications and pharmacological interventions to achieve optimal blood pressure control and reduce cardiovascular risk. These guidelines serve as a framework for healthcare professionals, including NPs, to deliver standardized, quality care, emphasizing the importance of individualized treatment plans based on client characteristics and comorbidities. 
Learn by Applying 
Apply what you have learned to the clinical scenarios below.  
Each client has an appointment to discuss issues related to the management of their hypertension. Select the most appropriate management plan for each client using the CPGs for hypertension and your textbook for drug names and dosages.
Client One: Malia Mowry
Examine the image below to learn more about the client to help you write an appropriate and individualized prescription.

Malia Mowry Image Description
Malia Mowry, a 40-year-old female client (DOB: 4/2/1984) has just been diagnosed with hypertension. Her physical exam reveals she is healthy with lab results in normal limits. 
Past Medical History: Asthma 
Allergies: Penicillin 
Medications: albuterol inhaler PRN for asthma exacerbation 
Social History: Quit smoking 2 years ago. Drinks 2 alcoholic beverages twice a month. 
Physical Exam:  
• Height: 5 ft 6 inches 
• Weight: 154 lbs 
• Body Mass Index (BMI): 24.9
• Blood Pressure (BP): 156/87
• Heart Rate (HR): 89
• Respiratory Rate (RR): 18
• Oxygen Saturation (O2SAT): 97% on RA 
• Temperature (TEMP): 98.6 oral
Write an appropriate prescription for this client in the activity below. Click the "Show Answers" option that will appear once all fields are complete to compare your response with the correct answer.

Patient Prescription Transcript
An appropriate prescription for Malia is: 
Name: Malia Mowry 
Date Of Birth: 04/02/1984 
Date Prescribed: Current Date
Rx: hydrochlorothiazide (HCTZ) 25mg  
Disp: 30
Sig: Take one tablet by mouth daily 
Refills (0-4): 1
Dispense as Written: 
Generic Substitution Permitted: 
• Either Dispense as Written or Generic Substitution Permitted should be checked on every written prescription depending on what is best for each client.  Refer to the week 1 lesson for criteria.  
Rationale: HCTZ is the first-line treatment for newly diagnosed hypertension. The client’s labs are normal, indicating that HCTZ is appropriate, as it requires adequate kidney function to work. Doses should be started low with follow-up assessment in one month, so only one refill is indicated pending reassessment (Whelton et al., 2018). 
Client Two: Raymond Collins
Examine the image below to learn more about the client to help you write an appropriate and individualized prescription. 

Raymond Collins Image Description
Raymond Collins, a 76-year-old male (DOB: 7/9/1948) presents to the clinic with high blood pressure at home for the past few weeks, despite attempting blood pressure reductions through medication compliance and lifestyle modifications. His physical exam reveals he is awake, alert, and oriented X 4. His exam is otherwise unremarkable, and his lab results indicate a decreased potassium level. His blood pressure averages over the past three visits have remained above 130 systolic.  
Past Medical History: Hypertension
Allergies: Aspirin
Medications: hydrochlorothiazide (HCTZ) 25mg PO daily  
Social History: He does not drink alcohol and quit smoking 20 years ago.  
Physical Exam:  
• Height: 5 ft 11 inches
• Weight: 198 lbs
• Body Mass Index (BMI): 27.6
• Blood Pressure (BP): 137/86
• Heart Rate (HR): 91
• Respiratory Rate (RR): 19
• Oxygen Saturation (O2SAT): 96% on RA
• Temperature (TEMP):  98.5 oral
Write an appropriate prescription for this client in the activity below. Click the "Show Answers" option that will appear once all fields are complete to compare your response with the correct answer.
 

Patient Prescription Transcript
An appropriate prescription for Raymond is: 
Client Name:  Raymond Collins 
Date of Birth: 7/9/1948 
Date Prescribed: Current Date 
Medication Name and Strength:  lisinopril (Zestril) 10mg  
Quantity:  30 
Directions: Take one tablet by mouth once daily 
Refills (0-4): 2 
Dispense as Written: 
Generic Substitution Permitted: 
• Either Dispense as Written or Generic Substitution Permitted should be checked on every written prescription depending on what is best for each client.  Refer to the week 1 lesson for criteria.  
Rationale: This older adult client has an average systolic blood pressure over 130, necessitating continued treatment according to the CPG. He currently takes HCTZ and has a low potassium level, reflecting potassium depletion, a known side effect of HCTZ. Adding an ACE inhibitor (lisinopril) is recommended by the CPG to help to further decrease blood pressure and help the client maintain normal potassium levels (Whelton et al., 2018). 

Arrhythmias can range from mild to life-threatening and can significantly impact cardiac output as well as increase morbidity and mortality. Various antiarrhythmics can be used to manage arrhythmias, with specific drugs indicated for specific arrhythmias. All antiarrhythmics can also cause arrhythmias, meaning all providers should carefully consider the risks and benefits for each individual client and circumstance and exercise caution when prescribing. Arrhythmias like atrial fibrillation also predispose clients to thromboembolic conditions with anticoagulation required for these clients, as well as for other indications (Rosenthal & Burchum, 2021). 

Management of Arrhythmias 
Managing arrhythmias requires a comprehensive approach to medication therapy using one or more of the below drug classes. Medication selection is influenced by assessment of the arrhythmia present, an individual's overall health, comorbidities, and other specific health needs. The choice of medication should be tailored to the individual client, aiming to effectively manage their specific arrhythmia while minimizing side effects. The following drug classes offer multiple mechanisms to influence cardiac rhythm (Rosenthal & Burchum, 2021). 
Click each section below to learn more about drugs used to manage arrhythmias. 
Class IA Antiarrhythmics: Sodium Channel Blockers
Class IA antiarrhythmics modulate the cardiac sodium channels to manage a variety of arrhythmias.
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Overview of the Drug
Prototype: quinidine (Cardioquin) 
• Category: Class IA Antiarrhythmics (Sodium Channel Blockers) 
• Primary Function: Class IA drugs block sodium channels in the myocardium to delay repolarization and moderate the action potential. 
• Unique Features: Used for atrial fibrillation, atrial flutter, and some ventricular arrhythmias. Not as widely used today due to safety concerns. 
Mechanism of Action
• Block sodium channels in the myocardium to reduce impulse conduction through the atria, ventricle, and His-Purkinje fibers and prolong the effective refractory period in atrial and ventricular myocardium. 
• Additionally, it increases vagal simulation to increase SA and AV node automaticity. To mitigate excessive stimulation of the ventricles, common practice involves pre-treatment with drugs like digoxin, verapamil, or beta blockers. These medications are effective in inhibiting AV (atrioventricular) conduction, thereby controlling the heart's response. 
Indications and Therapeutic Uses
• Arrhythmias: Used for supraventricular (atrial fibrillation, atrial flutter, and SVT) and some ventricular arrhythmias (ventricular tachycardia).
• Malaria: Quinidine is also the drug of choice for treating malaria.
Side Effects and Adverse Reactions
Side Effect Description
Diarrhea Many clients are affected by this GI symptom that causes many clients to discontinue treatment. This can potentially be avoided by taking with food.
Cinchonism (a cluster of dose-related side effects of quinine) This can develop in only one dose and includes tinnitus, headache, vertigo, and vision alterations.
Cardiotoxicity A prolonged QT interval is a warning sign. This can cause sinus arrest, AV block, ventricular tachydysrhythmias, or asystole.
Arterial Embolism When treating atrial fibrillation, clots can dislodge once normal sinus rhythm is restored. This is mitigated by beginning anticoagulants a few weeks before initiating treatment.
Hypotension Due to some alpha-adrenergic blocking effects, vasodilation can occur causing this. This occurs more frequently with IV routes of administration.
Hypersensitivity Fever, anaphylactic reactions, and thrombocytopenia can occur.
Precautions and Contraindications
Precautions
• To mitigate excessive stimulation of the ventricles, common practice involves pre-treatment with drugs like digoxin, verapamil, or beta blockers to inhibit AV conduction, thereby controlling the heart's response. 
• Caution in clients with impaired liver function. 
• Reduce digoxin doses and monitor for toxicity when administering with quinidine. 
Contraindications
• Avoid in clients with heart block or severe heart failure. 
• Avoid in clients with prolonged QT intervals. 
Black Box Warning
• Can increase mortality in clients with atrial fibrillation and atrial flutter. 
Drug Interactions
• Quinidine can increase the risk of [arrhythmias] and caution should be used when prescribing along with other [antiarrhythmic medications]. 
• Quinidine can double blood levels of [digoxin] due to displacing it from plasma albumin and decreasing elimination, potentially causing toxicity. 
• Drugs that induce hepatic metabolism can decrease the half-life of quinidine, including drugs like [phenobarbital] and [phenytoin]. 
• Quinidine can intensify the effects of [warfarin]. 
Dosing, Administration, & Client Teaching
Dosing
• Available as quinidine sulfate (immediate and sustained release tablets) and quinidine gluconate (sustained release oral tablets and parenteral solutions).  
• Dose is adjusted based on therapeutic levels and ECG findings. 
• Check drug dosing guidelines for individualized dosing. 
• Dose adjustment may be necessary in hepatic impairment. 
• Therapeutic plasma drug level range is between 2 and 5 mcg/mL. 
• Consider pre-treatment with drugs like digoxin, verapamil, or beta blockers to avoid excessive ventricular stimulation. 
• Consider pre-treatment with anticoagulants in atrial fibrillation. 
• Consider interactions with digoxin and the necessity of dosage adjustment. 
Administration
• Oral and IV forms available. 
Client Teaching
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Monitor blood pressure regularly, especially after initiating therapy. 
Labs to Monitor
Liver Function Tests (LFTs)
• Regular liver function tests may be required for certain clients. 
Serum Drug Levels
• Serum quinidine level with goal between 2 and 5 mcg/mL. 
• Serum drug levels for digoxin, if applicable. 
Class IB and IC Antiarrhythmics: Sodium Channel Blockers
Class IB and IC antiarrhythmics block sodium channels to manage ventricular arrhythmias.  
 Lidocaine
Lidocaine (Xylocaine) is a class II antiarrhythmic that is also a local anesthetic and will be covered more in-depth in the week 3 lesson. As an antiarrhythmic, its primary function is as an emergency medication to treat ventricular arrhythmias through IV administration in acute settings. It selectively blocks sodium channels, which are critical in cardiac conduction. It is important to differentiate lidocaine from licocaine with epinephrine, which is never given IV and reserved for local anesthesia in some circumstances.  
Flecainide
Class IC antiarrhythmics, with flecainide (Tambocor) as a prototype, are notable for their potent sodium channel blocking properties. These drugs are primarily used to manage severe ventricular arrhythmias and are effective in slowing conduction across various parts of the heart, including the atrial, ventricular, and His-Purkinje systems. They are beneficial for treating severe symptomatic ventricular arrhythmias and atrial fibrillation or flutter in clients without structural heart disease. Side effects may include visual disturbances, dizziness, and dyspnea, and they pose a heightened risk of proarrhythmic effects, particularly in clients with structural heart disease. Contraindications include recent myocardial infarction (MI) and significant bradycardia or sinus node dysfunction. These drugs can interact with other cardiac depressants and are potentiated by inhibitors of CYP2D6. Administration is oral, with dosing individualized for response and tolerance, and requires regular ECG monitoring and monitoring of liver and renal functions, especially for long-term use. Due to the potential for serious side effects, flecanide has a black box warning and should be reserved for severe ventricular arrhythmias that have not responded to safer drugs. 
Examine the image below to review normal cardiac conduction to apply the mechanism of action for class IC sodium channel blockers. 

Cardiac Conduction System Image Description
Title: Cardiac Conduction System
(The sequence of electrical conduction of the heart)
1. The sinoatrial (SA) node (pacemeaker) generate impulses
2. The impluses pause (0.1 s) at the artiventricular (AV) node.
3. The atrioventricular (AV) bundle connects the atria to the centricles.
4. The bundle branches conduct the impluses through the interventricular septum.
5. The Purkinje fibers depolarize the contractile cells of both ventricles.
• Network of specialized tissue that stimulates contractions. 
• Modified cardiac myocytes.
• The heart can contract without any innervation.
• Let atrium
• Left ventricle
• Purkinje fibers
• Interventricualr spetum
• Right ventricle
• Internodal pathway
• Right atrium
• Superior vena cava
Class II Antiarrhythmics: Beta Blockers
Class II antiarrhythmics are beta-blockers. Beta-blockers block sympathetic beta receptors to influence heart rate, heart rhythm, contractility, cardiac oxygen demand, and cardiac output, with potential effects on the respiratory system and glucose regulation as well, depending on the receptor selectivity of the medication. They are useful in treating arrhythmias due to their effects on the heart.
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Overview of the Drug
Prototypes: propranolol (Inderal) and metoprolol (Lopressor) 
• Category: Beta-blockers 
• Propranolol (Inderal) is a Nonselective Beta-blocker(affecting beta-1 and beta-2 adrenergic receptors and therefore the heart and lungs) 
• Metoprolol (Lopressor) is a Selective Beta-blocker (affect only beta-1 adrenergic receptor and therefore only the heart) 
• Primary Function: Block beta-1 adrenergic receptors in the heart to decrease heart rate, contractility, and conductivity to create an overall reduction in cardiac output and therefore blood pressure. 
• Unique Features: Subdivided into non-selective (beta-1 and beta-2) and selective (beta-1) blockers. All drugs in this class end in -olol. 
Mechanism of Action
• Non-Selective Beta Blockers: Block beta adrenergic receptors in the heart (beta-1) and the lungs (beta-2), leading to reduced heart rate, conductivity, and contractility and bronchoconstriction. 
• Selective Beta-1 Blockers: Block beta adrenergic receptors in the heart, reducing heart rate, force of contraction, and conduction velocity. These are beneficial to clients who could experience adverse health outcomes from beta-2 blockade (e.g., bronchoconstriction and hypoglycemia). 
Indications and Therapeutic Uses
• Hypertension: Blocking beta-1 adrenergic receptors in the heart decreases heart rate, contractility, and conductivity to create an overall reduction in cardiac output and, therefore, blood pressure.
• Angina: Blocking beta-1 adrenergic receptors in the heart decreases heart rate, contractility, and conductivity to decrease myocardial workload and, therefore, oxygen demand. 
• Arrhythmias: Blocking beta-1 adrenergic receptors in the heart decreases heart rate and conductivity through the SA and AV nodes to manage arrhythmias.
• Post MI: Reduces mortality and risk of subsequent MI due to reduction in cardiac oxygen demand from slowed heart rate and decreased contractility.
• Heart Failure: Some beta-blockers can be effective in improving morbidity by reducing myocardial workload for clients with some types of heart failure.
• Hyperthyroidism: Beta-blockers can control some symptoms of hyperthyroidism, such as tachycardia.
• Migraine Prophylaxis: Beta-blockers can reduce the frequency and severity of migraines (not indicated for acute treatment).
• Performance Anxiety: Beta-blockers can treat performance anxiety symptoms, including tachycardia, tremors, and sweating from SNS activation (“fight or flight”).
• Pheochromocytoma: Blocks the action of excessive catecholamine release and subsequent tachycardia associated with pheochromocytoma.
• Glaucoma: Topical beta-blockers can reduce intraocular pressure.
Side Effects and Adverse Reactions
Side Effect Description
Rebound Cardiac Excitation Abrupt withdrawal of beta-blockers can cause tachycardia and ventricular arrhythmias.
Reduced Cardiac Output Decreased heart rate, contractility, and conductivity could reduce this and precipitate or worsen heart failure.
Bradycardia, AV block Beta-blockers can compromise cardiac function in clients with certain cardiac dysfunction related to heart rate and rhythm. This could also cause hypotension.
Worsening Respiratory Status Non-selective beta blockers also block beta-2 receptors in the lungs, potentially causing bronchoconstriction. This means non-selective beta blockers (propranolol) are not indicated for clients with certain respiratory conditions.
Masking Hypoglycemia Normally, hypoglycemia causes an increase in heart rate. Blocking beta-1 receptors in the heart can block this tachycardic response and therefore cause this.
Hypoglycemia Normally, filling beta-2 receptors causes glycogenolysis. Blocking this with non-selective beta-blockers causes this alteration in blood sugar, which can be problematic for diabetic clients.
CNS reactions Beta-blockers cross the blood-brain barrier, rarely causing depression, insomnia, nightmares, or hallucinations.
Neonatal Symptoms Taking beta-blockers in pregnancy can predispose newborns to bradycardia, respiratory distress, and hypoglycemia since these drugs cross the placenta.
Precautions and Contraindications
Precautions
• Use cautiously in clients with depression since beta-blockers can cross the blood-brain barrier. 
• Monitor neonates of clients taking beta-blockers carefully for bradycardia, respiratory distress, and hypoglycemia. 
• Use caution with selective beta-blockers in diabetic clients due to beta-1 blockade that masks hypoglycemia symptoms (non-selective beta-blockers are contraindicated in diabetic clients). 
• Ensure the drug is not abruptly discontinued to prevent rebound cardiac excitation. 
• Use cautiously in heart failure. In HFrEF, beta blockers can worsen symptoms. 
Contraindications
• Contraindicated in clients with severe anaphylactic reactions that rely on epinephrine during anaphylaxis. Blocking beta receptors could prevent those sites from being filled with epinephrine when needed for anaphylaxis rescue use. 
• Contraindicated in clients with bradycardia and heart block. 
• Non-selective beta-blockers are contraindicated in clients with diabetes. 
• Non-selective beta-blockers are contraindicated in clients with respiratory conditions like asthma, COPD, emphysema, and chronic bronchitis. 
Black Box Warnings
• For sotalol (Betapace), clients must be monitored using ECG for three days and creatinine clearance must be checked before initiating. 
• For atenolol, metoprolol, nadolol, and timolol, abrupt discontinuation can cause angina or MI. 
Drug Interactions
• Taking beta-blockers with other antihypertensive drugs, especially [calcium channel blockers], can cause excessive cardiosuppression. 
• Taking [insulin] along with non-selective beta-blockers can cause hypoglycemia due to the ability of non-selective beta-blockers to prevent glycogenolysis to correct hypoglycemia. 
• Beta-blockers should be avoided in clients with a history of [anaphylaxis]because they block the effect of drugs like [epinephrine].  
Dosing, Administration, & Client Teaching
Dosing
• Dosage varies by indication and client response. 
• Check drug dosing guidelines for individualized dosing. 
• Oral, IV, and topical formulations available. 
• Gradual dosage adjustment recommended. 
Administration
• Oral administration is common and IV administration is available in acute settings. Topical administration is used to manage conditions like glaucoma. 
Client Teaching
• Importance of compliance and gradual withdrawal to avoid rebound cardiac excitation. 
• Monitor blood pressure and heart rate regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Monitoring for side effects including bradycardia, dizziness, breathing difficulties, or hypoglycemia. 
• Diabetic clients should regularly monitor blood sugar due to hypoglycemia masking.
Labs to Monitor
Basic Metabolic Panel (BMP) 
• Monitor blood glucose levels for diabetic clients (using BMP or POC glucose). 
Class III Antiarrhythmics: Potassium Channel Blockers
Class III antiarrhythmics are potassium channel blockers that prolong the cardiac action potential and are used to manage various types of arrhythmias.
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Overview of the Drug
Prototype: amiodarone (Cordarone)  
• Category: Class III Antiarrhythmic (Potassium Channel Blocker) 
• Primary Function: Block potassium channels, delaying repolarization and lengthening the action potential duration and refractory period in cardiac cells. Effective for atrial and ventricular arrhythmias. 
• Unique Features: Many toxicity risks are associated with amiodarone
Mechanism of Action
• These drugs block potassium channels during phase 3 of the cardiac action potential, prolonging the action potential duration and the refractory period, preventing rapid reactivation of the cardiac cells. 
Indications and Therapeutic Uses
• Arrhythmias: Used for atrial and ventricular arrhythmias, although it is only approved for ventricular arrhythmias.
Off-Label Uses
• Used off-label to manage atrial arrhythmias. 
Side Effects and Adverse Reactions
Side Effect/Adverse Reaction Description
Visual Disturbances Associated with optic neuropathy and optic neuritis, sometimes causing blindness.
Liver, Lung, and Thyroid Toxicity Can cause alterations in thyroid function, liver function, and lung function.
CNS Symptoms Ataxia, dizziness, tremors, and hallucinations.
Cardiotoxicity Amiodarone can cause arrhythmias through suppression of SA and AV node conduction, and precipitate heart failure.
Photosensitivity Reactions like photosensitivity can occur and turn skin blue-grey.
GI Reactions Nausea, vomiting, or anorexia are common.
Precautions and Contraindications
Precautions
• Requires careful monitoring in clients with lung and liver diseases, especially when using amiodarone.  
• If LFTs exceed three times the normal level, amiodarone should be discontinued.  
• If lung injury occurs, amiodarone should be discontinued. 
• Use with caution in clients with existing QT prolongation as amiodarone can further prolong the QT interval. 
Contraindications
• Contraindicated in clients with severe bradycardia, second or third-degree AV block, and severe hepatic impairment. 
• Contraindicated in pregnant and breastfeeding clients. 
• Metabolized by the CYP3A4 enzyme.  
Black Box Warnings
• Lung damage can occur, causing dyspnea and chest pain and resembling heart failure or pneumonia. Liver damage can also occur.
Drug Interactions
• Amiodarone has numerous [food and drug] interactions due to its impact on the CYP450 enzyme system. 
• Since amiodarone is metabolized by the [CYP3A4] enzyme, consuming [grapefruit juice] is contraindicated as it may cause amiodarone toxicity. 
• Amiodarone can increase the levels of several drugs, including [phenytoin, quinidine, digoxin, diltiazem, warfarin, some statins], etc.). 
• Drugs like [diuretics] and drugs that prolong the QT interval increase the risk of arrhythmias when taken with amiodarone.  
Dosing, Administration, & Client Teaching
Dosing
• Dose adjustment may be necessary in hepatic impairment. 
• Oral and IV formulations, with dosing depending on the indication and severity of the dysrhythmia. 
• Check drug dosing guidelines for individualized dosing. 
• Requires close monitoring of dosing due to its long half-life and potential for toxicity. 
• Initial treatment should occur within a hospital. 
• Loading and maintenance dosing available. 
• Long half-life and highly lipid soluble with many adverse effects. Use caution and reserve for use when other medications have not met client needs. 
Administration
• Administered orally or intravenously. 
• Avoid grapefruit juice. 
• IV administration requires cardiac monitoring. 
Client Teaching
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Monitor blood pressure and heart rate regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Educate clients about the importance of regular follow-up and lab monitoring. 
• Instruct on recognizing signs of lung, liver, and thyroid dysfunction. 
• Warn about the risk of sun exposure and the need for protective measures (specifically for amiodarone). 
• Emphasize the importance of reporting any visual changes, shortness of breath, or unusual fatigue. 
• Metabolized by CYP3A4 to teach about avoiding grapefruit juice. 
Labs to Monitor
Basic Metabolic Panel (BMP) 
• Regular monitoring of electrolytes, especially potassium. 
Serum Drug Levels 
• Serum drug levels of concurrent drugs, if applicable. 
Liver Function Tests (LFTs) 
• Liver function tests should be performed due to liver toxicity. 
Thyroid Studies 
• Thyroid levels at baseline and during treatment 
Class IV Antiarrhythmics: Calcium Channel Blockers
Class IV antiarrhythmics are calcium channel blockers that are non-dihydropyridines that relax blood vessels by inhibiting calcium from entering arterial cells and reduce conductivity, contractility, and heart rate by inhibiting calcium from entering cardiac muscle cells. Only the non-dihydropyridines are effective in managing supraventricular arrhythmias due to their effect on cardiac muscle cells.
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Overview of the Drug
Prototypes: verapamil (Calan) 
• Category: Calcium Channel Blockers 
• Verapamil (Calan) and diltiazem (Cardizem) are Non-dihydropyridine(affect the heart and blood vessels), making them useful for managing arrhythmias. 
• Primary Function: They inhibit the influx of calcium ions into myocardial and vascular smooth muscle cells, causing vasodilation and reducing cardiac workload. They control heart rate by slowing conduction through the AV node (non-dihydropyridines only).  
• Unique Features: Only non-dihydropyridines that affect the heart and blood vessels are useful for treating arrhythmias. They are effective in treating certain supraventricular tachyarrhythmias (atrial fibrillation, atrial flutter, SVT, etc.). 
Mechanism of Action
• Non-dihydropyridines bind calcium channels in the heart and blood vessels. This reduces afterload and cardiac workload, decreasing myocardial oxygen demands. 
• Heart: Binding calcium channels in cardiac myocytes and nodal tissue (SA and AV nodes) causes decreased contractility, decreased heart rate, and decreased conductivity 
• Blood Vessels: Binding calcium channels causes vasodilation. 
Indications and Therapeutic Uses
• Hypertension: Dilation of arterioles contributes to a reduction in blood pressure.
• Angina: Arteriole dilation reduces afterload and therefore decreases myocardial oxygen demand. They also relax coronary vasospasm, useful in variant (Printzmetal) angina.
• Arrhythmias: Suppressing conduction through the AV node can reduce the incidence of supraventricular tachycardias (atrial fibrillation, atrial flutter, and SVT).
Side Effects and Adverse Reactions
Side Effect/Adverse Reaction Description
Constipation This side effect happens from blocking calcium channels in intestinal smooth muscle and is more common in older adults taking non-dihydropyridines. This can be minimized by increasing dietary fiber and fluids.
Headache, flushing, peripheral edema, dizziness Can occur from vasodilation.
Bradycardia, AV block Non-dihydropyridines can compromise cardiac function in clients with certain cardiac dysfunction.
Precautions and Contraindications
Precautions
• Grapefruit juice can inhibit metabolism of many calcium channel blockers and potentially cause toxicity. 
• Use non-dihydropyridines cautiously in clients with heart failure. Clients with systolic heart failure (heart failure with reduced ejection fraction; HRrEF) can experience worsening heart failure due to decreased contractility. 
• Caution in elderly clients due to increased sensitivity and risk of side effects. 
• Dose adjustment may be necessary in clients with severe hepatic impairment. 
Contraindications
• Avoid non-dihydropyridines in clients with AV block, bradycardia, and heart failure with reduced ejection fraction. 
• Avoid in clients with severe hypotension or cardiogenic shock. 
• Pregnancy category C: Weigh risks and benefits in pregnant and breastfeeding clients. 
Drug Interactions
• [Beta-blockers and Digoxin] can increase the risk of bradycardia and AV block, especially when used with non-dihydropyridines. 
• [Grapefruit juice] consumption can increase levels of certain calcium channel blockers, leading to toxicity. 
Dosing, Administration, & Client Teaching
Dosing
• Oral administration, with doses varying depending on the specific drug and condition being treated. 
• Check drug dosing guidelines for individualized dosing. 
• Dose adjustment may be necessary in hepatic impairment. 
• Avoid non-dihydropyridines in clients with HFrEF due to their effects on contractility. 
• Formulations can be immediate release or extended-release for once-daily dosing. 
• Initiation at lower doses with gradual titration to minimize side effects. 
• Order calcium channel blockers and other cardiosuppressive drugs (e.g., digoxin, beta-blockers, etc.) several hours apart. 
Administration
• Oral administration. 
• Avoid grapefruit juice. 
• Administer calcium channel blockers and other cardiosuppressive drugs (e.g., digoxin, beta-blockers, etc.) several hours apart. 
Client Teaching
• Educate about potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and regular monitoring of blood pressure and heart rate. 
• Emphasize the avoidance of grapefruit juice while taking certain CCBs. 
• Advise clients to report symptoms like significant swelling, severe dizziness, or palpitations. 
• Monitor for signs of heart failure, especially in clients with pre-existing heart conditions. 
Labs to Monitor
Liver Function Tests (LFTs) 
• Regular liver function tests may be required for certain clients. 
Adenosine
Adenosine is a unique and powerful antidysrhythmic agent, primarily used in the emergency treatment of certain forms of supraventricular tachycardia (SVT). It works by slowing electrical conduction through the atrioventricular (AV) node, thereby interrupting the reentrant pathways that contribute to SVT. This action helps to restore normal sinus rhythm. Adenosine is administered intravenously and is known for its extremely short half-life, generally less than 10 seconds, which necessitates rapid administration. Upon administration, clients may experience transient side effects such as flushing, chest discomfort, or a sense of impending doom, but these usually resolve quickly. It's crucial for healthcare providers to closely monitor the client's cardiac rhythm and vital signs during and after its administration, given its potent and transient effects on the heart (Rosenthal & Burchum, 2021). 
Learn By Applying
Apply what you have learned to the clinical scenario below
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Molly Madison, a 45-year-old female with a history of hypertension, was recently diagnosed with an AV heart block. Which of the following medications is most appropriate to manage her hypertension? 
• Propranolol (Inderal) 
• Lisinopril (Zestril) (Correct answer) 
• Diltiazem (Cardizem) 
• Amiodarone (Cordarone) 
Rationale: Lisinopril acts on the RAAS to reduce blood pressure without directly acting on conduction through the myocardium. Propranolol (a non-selective beta-blocker) and diltiazem (a non-dihydropyridine calcium channel blocker) decrease heart rate, conductivity, and contractility, which could negatively impact a client with AV heart block. Amiodarone can suppress SA and AV node conduction which could also negatively impact a client with an existing heart block. 
Anticoagulants
Anticoagulants can be useful in managing many health conditions predisposing clients to thromboembolic events. They can be ordered and administered in a variety of settings as oral, subcutaneous, and intravenous formulations are available (Rosenthal & Burchum, 2021).  
Click each section below to learn more about anticoagulants. 
Oral Anticoagulants
Oral anticoagulants are useful to help clients manage conditions that predispose them to thromboembolic complications. 
Click each tab below to learn more about oral anticoagulants. 
Warfarin (Coumadin)
Warfarin is an anticoagulant that inhibits vitamin K-dependent clotting factors and is used to manage thromboembolic events.
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Overview of the Drug
Prototype: warfarin (Coumadin) 
• Category: Oral Anticoagulant (Vitamin K Antagonist) 
• Primary Function: It is used widely in the management of thromboembolic disorders, although it has a delayed onset so it is not appropriate for emergencies. 
• Unique Features: Warfarin is the oldest oral anticoagulant and requires frequent monitoring using PT/INR lab values. 
Mechanism of Action
• Warfarin interferes in the clotting cascade by inhibiting the synthesis of Vitamin K-dependent clotting factors, which are essential for blood clotting. These factors include Factors VII, IX, and X, and prothrombin. It acts by inhibiting the enzyme Vitamin K epoxide reductase complex 1 (VKORC1), which is crucial in the Vitamin K cycle.  
• Warfarin is highly bound to plasma albumin with any unbound drug able to readily cross membranes. Warfarin has no effect on clotting factors already in circulation as it only acts on the production of new clotting factors. This causes a delayed onset of action with the first effects occurring between 8-12 hours after initial administration with full anticoagulation effect happening days after initiation. Warfarin also has a long half-life (1.5-2 days) meaning anticoagulation effects continue after dosing stops. 
Indications and Therapeutic Uses
• Atrial Fibrillation: Used for prevention of thromboembolic events resulting from atrial fibrillation.
• Venous Thrombosis: Used for management of venous thrombosis to prevent further complications (e.g., pulmonary embolism).
• Pulmonary Embolism: Used for management of pulmonary embolism to prevent extension of clotting and recurrent clots.
• Heart Valve Replacement: Used for the prevention and treatment of thromboembolic complications associated with mechanical and tissue-based cardiac valve replacement.
• Post MI: Used for the reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction.
• Stroke and MI Prevention: Used for the reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction.
Side Effects and Adverse Reactions
Side Effect Description
Hemorrhage The major complication from warfarin therapy. This can occur anywhere in the body and is treated by administering vitamin K.
Increased Risk for Fractures Long-term use of warfarin (more than one year) is associated with this.
Skin Disturbances Responses like urticaria, skin necrosis, alopecia, or dermatitis may occur.
Precautions and Contraindications
Precautions
• Discontinue warfarin several days before surgery. Consider administering vitamin K if emergency surgery is indicated. 
• Caution in clients with high bleeding risks such as those with gastrointestinal ulcers, esophageal varices, thrombocytopenia, recent eye or brain trauma surgery, hemorrhagic stroke history, uncontrolled hypertension, and severe liver or kidney disease. 
Contraindications
• Contraindicated in pregnancy due to the risk of fetal bleeding and teratogenesis, especially during the first trimester. 
• Category X  
• Warfarin enters breast milk and is therefore contraindicated in breastfeeding. 
Black Box Warnings
• Bleeding risk and the necessity of regular monitoring of INR. 
• All anticoagulants can cause bleeding, with clients receiving spinal or epidural anesthesia being at risk for hematoma. 
Drug Interactions
• Warfarin interacts with drugs that increase its anticoagulant effects, including drugs that displace warfarin from albumin like [sulfonamides], drugs that inhibit warfarin degradation like [amiodarone and some antibiotics], and drugs that decrease the synthesis of clotting factors like some [parenteral cephalosporins]. 
• Warfarin interacts with drugs that promote bleeding, including drugs that inhibit platelet aggregation like [NSAIDs, aspirin, and other antiplatelets], drugs that inhibit clotting factors or thrombin like [heparin and direct thrombin inhibitors], and drugs that promote ulcer formation like [glucocorticoids and aspirin]. 
• Warfarin interacts with drugs that decrease its effects, including drugs that induce enzymes that metabolize warfarin like [phenytoin, rifampin, phenobarbital, and carbamazepine], drugs that promote clotting factor synthesis like [oral contraceptives or vitamin K], and drugs that reduce warfarin absorption like [cholestyramine]. 
• Certain foods rich in Vitamin K (e.g., [leafy green vegetables, mayonnaise, canola oil, and soybean oil]) can decrease the effectiveness of warfarin. 
• Warfarin interacts with many herbs starting with “G”, including [garlic, ginko, ginger, and ginseng], as well as feverfew, green tea, and fish oil. 
Dosing, Administration, & Client Teaching
Dosing
• Oral formulations and parenteral formulations available (although not frequently used). 
• Check drug dosing guidelines for individualized dosing. 
• Dose adjustment may be necessary in hepatic impairment. 
• Individualized dosing based on age, comorbidities, and concomitant medications. 
• INR monitoring with a goal INR between 2-3 in most clients, adjusting dosage as needed. 
• Discontinue 7 days before surgery. 
• Reverse anticoagulation effects with vitamin K (phytonadione). 
• Some genotypes (particularly Asian clients) may require lower starting doses of warfarin and genetic testing is available. 
• Subtherapeutic (=3 in women); therefore, anticoagulation is recommended according to the CPG. The CPG recommends DOACs over warfarin to reduce this risk (Joglar et al., 2024). Due to the client’s renal insufficiency, direct thrombin inhibitors like dabigatran may be more appropriate than factor Xa inhibitors, which should be avoided in severe renal insufficiency, although dabigatran will need to be renally dosed. Since the client’s creatinine clearance is between 15-30 mL/min, dabigatran is started at 75mg twice per day. Since the client is being switched from warfarin to dabigatran, the provider should wait until the INR is below 2 to authorize the client to begin dabigatran to avoid an increased risk of bleeding (Rosenthal & Burchum, 2021). The client only has one refill as the provider will want to re-evaluate them quickly to ensure there are no adverse reactions. 
Client Two: Arthur King
Examine the image below to learn more about the client to help you write an appropriate and individualized prescription

Arthur Green Image Description
Arthur King, a 65-year-old male (DOB: 10/5/1959), presents to the clinic today one day after discharge from the hospital with a new diagnosis of atrial fibrillation in need of medication for anticoagulation while waiting for an ablation. His labs indicate normal renal function, stable blood sugar, and an INR of 1. His physical exam is unremarkable. 
Past Medical History: Type 2 Diabetes, Hypertension, Heart Failure with preserved ejection fraction (HFpEF)
Allergies: Aspirin
Medications: hydrochlorothiazide (HCTZ) 25mg PO daily, glucophage (Metformin) 500mg PO BID, captopril (Capoten) 25mg PO q12hr, and verapamil (Calan) 120mg PO TID 
Social History: The client drinks 4-5 drinks per week and quit smoking 5 years ago. 
Physical Exam:  
• Height: 5 ft 10 inches
• Weight: 250 lbs
• Body Mass Index (BMI): 35.9
• Blood Pressure (BP):  126/79
• Heart Rate (HR): 84 (Afib)
• Respiratory Rate (RR): 16
• Oxygen Saturation (O2SAT): 95% on RA
• Temperature (TEMP): 98.5 oral
Write an appropriate prescription for this client in the activity below. Click the “Show Answers” option that will appear once all fields are complete to compare your response with the correct answer.

Patient Prescription Transcript
An appropriate prescription for Arthur is:
Client Name:  Arthur King 
Date of Birth: 10/5/1959 
Date Prescribed: Current Date 
Medication Name and Strength:  rivaroxaban (Xarelto) 20mg 
Quantity:  30 
Directions: Take one 20mg tablet by mouth daily with dinner 
Refills (0-4): 1 
Dispense as Written: 
Generic Substitution Permitted: 
• Either Dispense as Written or Generic Substitution Permitted should be checked on every written prescription depending on what is best for each client.  Refer to the week 1 lesson for criteria.  
Rationale: The client’s CHA2DS2-VASc2 score of 4 places the client in a high-risk category for thromboembolism, meaning anticoagulation is recommended according to the CPG. The CPG recommends DOACs over warfarin to reduce this risk (Joglar et al., 2024). With direct thrombin inhibitors like dabigatran, drugs that inhibit P-glycoprotein (like verapamil that the client is taking) can increase dabigatran absorption and blood levels and therefore increase bleeding so they would not be the best choice in this client. Although verapamil can moderately inhibit CYP3A4 and P-glycoprotein and increase the risk of bleeding in clients with renal impairment, that consideration does not apply to this client since he has normal renal function. Therefore, rivaroxaban would be an appropriate DOAC for this client to prevent thrombosis related to atrial fibrillation (Rosenthal & Burchum, 2021). 

Coronary artery disease affects millions of Americans and can contribute to many conditions that increase morbidity and mortality. Managing lipid levels is critical to advancing the health of clients with impaired coronary perfusion. Impaired coronary perfusion can cause angina or myocardial infarction, requiring pharmacologic management of angina with various medications to optimize health outcomes for these clients as well (Rosenthal & Burchum, 2021). 

Management of Lipids 
Managing lipid levels requires a comprehensive approach to nonpharmacologic interventions (including diet) and medication therapy using one or more of the below drug classes. Medication selection is influenced by the assessment of an individual’s overall health, comorbidities, and other specific health needs. The choice of medication should be tailored to the individual client, aiming to effectively manage lipid levels while minimizing side effects. The following drug classes offer multiple mechanisms to address elevated lipid levels (Rosenthal & Burchum, 2021).  
Click each section below to learn more about drugs used to manage lipids. 
Statins
Statins, formally known as HMG-CoA reductase inhibitors, inhibit the enzyme HMG-CoA reductase to lower cholesterol.
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Overview of the Drug
Prototype: lovastatin (Mevacor) 
• Category: HMG-CoA Reductase Inhibitors (aka Statins) 
• Primary Function: Statins are a class of lipid-lowering medications primarily used to reduce cholesterol levels in the blood, particularly low-density lipoprotein (LDL) cholesterol, which is often referred to as “bad” cholesterol. 
• Unique Features: These drugs are referred to as “statins” because the generic name ends in -statin. 
Mechanism of Action
• Statins inhibit the enzyme HMG-CoA reductase in the liver. This enzyme is crucial for the synthesis of cholesterol. By inhibiting this enzyme, statins effectively reduce the production of cholesterol, leading to decreased levels of LDL cholesterol in the body. 
Indications and Therapeutic Uses
• Hypercholesterolemia: Statins are the most effective drug for decreasing LDL cholesterol.
• Post MI: Used for the reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction.
• Stroke and MI Prevention: Prevention of cardiovascular events in clients with a high risk of developing heart disease, including diabetic clients. 
Side Effects and Adverse Reactions
Side Effect Description
Hepatotoxicity Increased liver enzymes indicating potential liver damage.
Myopathy and Rhabdomyolysis A severe breakdown of muscle tissue that can lead to kidney damage. Monitor CK lab values to determine if muscle breakdown is occurring and kidney function labs and urine studies to determine kidney function.
Precautions and Contraindications
Precautions
• Perform liver function tests prior to initiating treatment and then when clinically indicated. 
• Caution in clients with a history of liver disease or heavy alcohol use. 
• Statins should be used cautiously in elderly clients due to increased risk of muscle-related side effects. 
• Consider the use of certain statins in clients of Asian descent (particularly rosuvastatin) as toxicity can occur from altered metabolism. 
Contraindications
• Absolute contraindication in pregnancy due to the risk of congenital defects.
Drug Interactions
• Combining a stating with other lipid-lowering medications (including [fibrates]) can increase the risk of myopathy and hepatotoxicity. 
• Statins are metabolized by CYP3A4 so drugs and foods that inhibit this enzyme, including [grapefruit juice, macrolide antibiotics, azole antifungals, and amiodarone], can increase statin levels. 
Dosing, Administration, & Client Teaching
Dosing
• Dose adjustment may be necessary in hepatic impairment. 
• Check drug dosing guidelines for individualized dosing. 
• Statins are typically administered once daily. The timing of the dose may vary, but evening administration is common for certain statins due to the body’s natural rhythm of cholesterol production. 
• Dosage is adjusted based on the client’s LDL levels, tolerance, and response to the medication. 
• Monitor CK, LFTs, and cholesterol levels. 
Administration
• Oral administration. 
• Typically administered at night since most cholesterol synthesis occurs at night and these drugs inhibit that process. 
Client Teaching
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Avoid grapefruit juice. 
• Inform about potential side effects and the importance of reporting muscle pain or weakness. 
• Discuss the necessity of routine blood tests to monitor liver function and cholesterol levels. 
• Highlight the importance of maintaining a healthy diet and exercise regimen alongside medication. 
Labs to Monitor
Liver Function Tests (LFTs)
• Monitor liver function tests (LFTs) prior to treatment and to monitor for hepatotoxicity. 
Creatine Kinase (CK)
• Assess creatine kinase (CK) levels if symptoms of myopathy or muscle pain occur. 
Lipid Profiles
• Regularly monitor lipid profiles to assess effectiveness. 
Basic Metabolic Panel (BMP)
• Assess kidney function if myopathy and rhabdomyolysis is suspected. 
Fibric Acid Derivatives
Fibric acid derivatives lower triglyceride levels and moderately reduce LDL cholesterol and are used to manage hypertriglyceridemia.
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Overview of the Drug
Prototype: gemfibrozil (Lopid) 
• Category: Fibric Acid Derivatives (a.k.a. Fibrates) 
• Primary Function: Fibric acid derivatives, commonly known as fibrates, are a class of medications primarily used to lower lipid levels, specifically triglycerides, and to a lesser extent, increase high-density lipoprotein (HDL) cholesterol. 
• Unique Features: The principle indication for fibrates is hypertriglyceridemia and treatment is reserved for clients who have not responded to weight control and diet modifications.
Mechanism of Action
• Fibrates activate peroxisome proliferator-activated receptors (PPARs), specifically PPAR-alpha. This activation leads to an increase in the oxidation of fatty acids in the liver and muscle tissue. They decrease the production of triglycerides and VLDL (very low-density lipoprotein) while increasing HDL cholesterol. 
Indications and Therapeutic Uses
• Hypertriglyceridemia: Primarily prescribed for the treatment of high triglyceride levels (hypertriglyceridemia).
Side Effects and Adverse Reactions
Side Effect Description
Gallstones Since fibrates increase biliary cholesterol saturation, they predispose clients to gallstones.
Hepatotoxicity Increased liver enzymes indicating potential liver damage.
Myopathy and Rhabdomyolysis A severe breakdown of muscle tissue that can lead to kidney damage. Monitor CK lab values to determine if muscle breakdown is occurring and kidney function labs and urine studies to determine kidney function.
Precautions and Contraindications
Precautions
• Use with caution in clients with a history of gallbladder disease. 
• Should be used with extreme caution or avoided in combination with statins due to increased risk of myopathy and rhabdomyolysis and hepatotoxicity. 
Contraindications
• Contraindicated in clients with severe liver disease. 
• Not recommended in clients with severe renal impairment. 
Drug Interactions
• Concurrent use with [statins] increases the risk of myopathy, rhabdomyolysis, and hepatotoxicity. 
• Gemfibrozil displaces [warfarin] from plasma albumin, increasing the risk of bleeding. 
Dosing, Administration, & Client Teaching
Dosing
• Oral administration. 
• Dose adjustment may be necessary in hepatic impairment. 
• Check drug dosing guidelines for individualized dosing. 
• The dosage varies based on the specific medication and client’s response. 
• Usually taken once or twice daily with meals to enhance absorption and reduce gastrointestinal side effects. 
• Monitor liver function and cholesterol levels and CK levels if muscle injury is suspected. 
Administration
• Oral administration. 
Client Teaching
• Educate about lifestyle changes, including diet and exercise, to enhance the drug’s effectiveness. 
• Advise patients to report any unusual muscle pain, tenderness, or weakness, especially if taking statins concurrently. 
• Discuss the importance of regular follow-up appointments and blood tests to monitor triglyceride levels and liver function. 
Labs to Monitor
Liver Function Tests (LFTs)
• Monitor liver function tests (LFTs) prior to treatment and to monitor for hepatotoxicity. 
Creatine Kinase (CK)
• Assess creatine kinase (CK) levels if symptoms of myopathy or muscle pain occur. 
Lipid Profiles
• Regularly monitor lipid profiles to assess effectiveness. 
Bile Acid Sequestrants
Bile acid sequestrants lower LDL cholesterol levels by binding bile acids in the intestine.
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Overview of the Drug
Prototype: colesevelam (Welchol) 
• Category: Bile Acid Sequestrants 
• Primary Function: Bile acid sequestrants work by binding to bile acids in the intestine, preventing their reabsorption and therefore decreasing LDL cholesterol. 
• Unique Features: Often used as an adjunct to statins or when statins are contraindicated or not tolerated. 
Mechanism of Action
• Bile acid sequestrants work by binding to bile acids in the intestine, preventing their reabsorption. This leads to an increased excretion of bile acids in the stool. To compensate, the liver converts more cholesterol into bile acids, thus lowering circulating cholesterol levels. 
Indications and Therapeutic Uses
• Hypercholesterolemia: Bile acid sequestrants are useful as an adjunct to statin therapy for decreasing LDL cholesterol.
Side Effects and Adverse Reactions
Side Effect Description
Constipation The most common complaint that can be minimized by increasing fiber and fluids.
Decreased Absorption of Fat-Soluble Vitamins May interfere with the absorption of fat-soluble vitamins (A, D, E, K), although that is more common in older bile acid sequestrants.
Precautions and Contraindications
Precautions
• Caution in clients with a history of chronic constipation or bowel motility issues. 
• Use with caution in clients with a tendency to vitamin deficiencies. 
Contraindications
• Contraindicated in individuals with complete biliary obstruction. 
Drug Interactions
Bile acid sequestrants can bind to and reduce the absorption of many drugs, including [thiazide diuretics, digoxin, warfarin, and some antibiotics]. 
Timing of administration should be adjusted to avoid interaction with other medications, either [1 hour] before the bile acid sequestrant or [4 hours] after. 
Dosing, Administration, & Client Teaching
Dosing
• Administered as tablets and a powder for oral suspension. 
• Dosage varies based on the specific agent and client’s response. 
• Check drug dosing guidelines for individualized dosing. 
• Usually taken with meals to bind the bile acids released during digestion. 
• Clients may require supplementation with fat-soluble vitamins. 
Administration
• Administered as tablets and a powder for oral suspension. 
• Take with food and water. 
Client Teaching
• Educate clients on the importance of maintaining a regular medication schedule. 
• Advise about the potential for gastrointestinal side effects and ways to manage them. 
• Instruct clients to take other medications at a different time than bile acid sequestrants to prevent interaction. 
• Discuss dietary changes to manage constipation and ensure adequate vitamin intake. 
Labs to Monitor
Lipid Profiles
• Regularly monitor lipid profiles to assess effectiveness. 
 Niacin, ezetimibe (Zetia), and Monoclonal Antibodies
Niacin, ezetimibe (Zetia), and monoclonal antibodies are other drugs used for managing cholesterol. Niacin, also known as Nicotinic Acid, is a unique lipid-altering medication that significantly lowers LDL and triglyceride levels while raising HDL levels. Recent studies have demonstrated that niacin did not significantly improve clinical outcomes, so it is not as widely prescribed. Niacin works by inhibiting the synthesis of triglycerides in the liver and adipose tissue, thus reducing VLDL and consequently LDL levels. It is available in multiple formulations, each varying in side effect profiles. Common adverse effects include intense skin flushing, gastrointestinal upset, and potential liver injury. Regular monitoring of liver function is recommended due to potential hepatotoxicity. Niacin also serves as a vitamin at much lower doses than those used for lipid management (Rosenthal & Burchum, 2021). 
Ezetimibe (Zetia) is a distinct cholesterol-reducing medication that functions by blocking cholesterol absorption in the small intestine. This action lowers the levels of total cholesterol, LDL, and triglycerides in the plasma while potentially causing a minor increase in HDL cholesterol. Ezetimibe is taken orally and is used alongside dietary changes to manage hypercholesterolemia. It can be administered as a standalone treatment or combined with statins, enhancing the LDL reduction effect. Although well-tolerated with a low incidence of significant side effects, rare cases of myopathy and hepatotoxicity have been reported. Ezetimibe’s interactions with other drugs, such as statins and fibrates, should be carefully monitored, particularly regarding liver function and myopathy risks (Rosenthal & Burchum, 2021).  
Monoclonal antibodies like alirocumab (Praluent) and evolocumab (Repatha), represent a novel approach in treating clients with high LDL cholesterol levels, particularly those with familial hypercholesterolemia or atherosclerotic cardiovascular disease. These drugs function by inhibiting PCSK9, a protein that typically binds to LDL receptors in the liver, hindering their ability to clear LDL cholesterol from the blood. By blocking PCSK9, LDL receptors are more available to remove LDL cholesterol, effectively lowering its levels in the bloodstream. Administered subcutaneously, these inhibitors have a long half-life and are generally well-tolerated, although they may cause hypersensitivity reactionsin some cases. They are used in conjunction with diet changes and statin therapy to optimize cholesterol reduction. 
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• Jane Phelps reports right upper quadrant (RUQ) pain and “feeling achy all over”. She has a history of high cholesterol and is taking atorvastatin. Which of the following assessment parameters are important to consider? Select all that apply. 
• Liver function tests (Correct answer)
• Creatine kinase (Correct answer)
• BUN (Correct answer)
• Creatinine (Correct answer)
• Jaundice (Correct answer)
• Grapefruit juice consumption (Correct answer)
Rationale: Statins, such as atorvastatin, can cause hepatotoxicity, myopathy, and potentially rhabdomyolysis. Assessing liver function tests and the presence of jaundice is helpful in identifying signs of hepatotoxicity. Assessing BUN and creatinine can be helpful in determining adequate kidney function relative to rhabdomyolysis. Assessing creatine kinase (CK) can be helpful in identifying myopathy. Grapefruit juice is a CYP3A4 inhibitor and can cause toxicity related to statins and should also be assessed. 

Management of Angina 
Managing angina through pharmacologic therapy involves a careful strategy to prevent myocardial infarction (MI) and death, while also alleviating anginal pain. This approach primarily focuses on balancing oxygen supply and demand within the heart. Key medications include nitrates, which help dilate blood vessels to improve the oxygen supply and reduce oxygen demand, and beta-blockers, which reduce heart rate and contractility and, therefore, myocardial demand for oxygen. Long-term management often includes a combination of lifestyle changes and ongoing medication (Rosenthal & Burchum, 2021). 
Click each section below to learn more about drugs used to manage angina. 
Nitrates
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Overview of the Drug
Prototype: nitroglycerin
• Category: Nitrate 
• Primary Function: Nitrates are vasodilators used primarily in the treatment of angina pectoris. They act on both arterial and venous vessels. 
• Unique Features: Nitroglycerin has been prescribed for angina since 1879 and comes in multiple formulations (sublingual tablet, sublingual spray, IV, transdermal, etc.). 
Mechanism of Action
• Nitrates relax vascular smooth muscle through conversion to nitric oxide. This causes venous and arterial dilation (in higher doses), reducing preload and afterload on the heart, thus lowering myocardial oxygen demand. 
Indications and Therapeutic Uses
• Angina: Primarily used for relief of angina symptoms. This includes acute management of anginal attacks and prophylaxis of angina pectoris in clients with stable angina.
Side Effects and Adverse Reactions
Side Effect Description
Headache The most common side effect from initial treatment.
Reflex tachycardia This can happen due to reflex increase in sympathetic activity related to a fast drop in cardiac output from vasodilation.
Orthostatic Hypotension Sudden drop in blood pressure upon standing. This can cause dizziness or syncope.
Precautions and Contraindications
Precautions
• Use cautiously in clients with head trauma or cerebral hemorrhage due to intracranial pressure effects. 
• Tolerance can develop quickly (within 24 hours). Ensure drug holidays (usually at night). 
• Reflex tachycardia can develop from rapidly dropping blood pressure and administration of beta blockers and non-dihydropyridine calcium channel blockers can manage it. 
Contraindications
• Contraindicated in clients with severe hypotension or hypersensitivity to nitrates. 
• Avoid in clients taking phosphodiesterase inhibitors (e.g., sildenafil) due to risk of severe hypotension. 
Drug Interactions
• Using nitrates with [phosphodiesterase inhibitors (e.g., Viagra, Cialis)] can cause severe hypotension. 
• Nitrates may interact with other [antihypertensive drugs], enhancing their effect. 
Dosing, Administration, & Client Teaching
Dosing
• Available in many formulations including sublingual tablets, sublingual spray, transdermal, IV, etc. 
• Check drug dosing guidelines for individualized dosing. 
• Sublingual forms for acute attacks: Take one tablet at the onset of chest pain, may take additional doses every 5 minutes, up to three doses. If pain persists 5 minutes after the first SL dose, seek emergency medical assistance. 
• Immediate and sustained release formulations are available in PO form (isosorbide mononitrate and isosorbide dinitrate). 
• The MONA (Morphine, Oxygen, Nitrates, Aspirin) protocol is commonly employed in acute cases to quickly address symptoms, prevent further cardiac damage, and reduce the risk of life-threatening complications 
Administration
• Ensure sublingual tablets are not swallowed. 
• For transdermal patches or pastes for prophylaxis, apply as directed, typically once daily. Rotate sites and allow drug-free intervals to prevent tolerance. 
• The MONA (Morphine, Oxygen, Nitrates, Aspirin) protocol is commonly employed in acute cases to quickly address symptoms, prevent further cardiac damage, and reduce the risk of life-threatening complications 
Client Teaching
• Teach clients how to use sublingual forms for acute attacks: Take one tablet at the onset of chest pain, may take additional doses every 5 minutes, up to three doses. If pain persists 5 minutes after the first SL dose, seek emergency medical assistance. 
• Teach clients about the importance of properly taking SL tablets. They are ineffective if swallowed. 
• Educate about the potential for headaches, orthostatic hypotension, and importance of adherence to regimen. 
Labs to Monitor
• Regular lab monitoring is not typically required for nitrate therapy.  
Intravenous Nitroglycerin
Intravenous (IV) nitroglycerin is a potent vasodilator widely used in the management of acute episodes of angina pectoris, particularly in the setting of acute coronary syndromes and myocardial infarction. The primary action of IV nitroglycerin is to relax vascular smooth muscle, resulting in dilation of both arterial and venous blood vessels. This dual action leads to a decrease in preload and afterload on the heart, effectively reducing myocardial oxygen demand and alleviating chest pain associated with angina (Rosenthal & Burchum, 2021). 
When administered intravenously, nitroglycerin allows for rapid onset of action and precise titration of dosage, which is crucial in managing acute cardiac conditions. The administration of IV nitroglycerin requires close monitoring of the client’s hemodynamic status, including blood pressure and heart rate, due to the drug’s potent effects on the cardiovascular system. Hypotension and reflex tachycardia are potential side effects, necessitating careful monitoring and adjustment of the infusion rate as needed (Rosenthal & Burchum, 2021). 
IV nitroglycerin is typically administered in a critical care setting, such as a coronary care unit or emergency department, where continuous cardiac monitoring can be provided. Nurses and healthcare providers must also be aware of the drug’s interactions, particularly with phosphodiesterase inhibitors, which can lead to severe hypotension. Overall, IV nitroglycerin is a critical component in the management of acute anginal episodes, offering rapid and effective relief of chest pain by decreasing cardiac workload and improving coronary blood flow (Rosenthal & Burchum, 2021). 
Antiplatelets
Antiplatelet medications help reduce thrombus formation in the coronary arteries by inhibiting platelet aggregation, thereby improving blood and oxygen delivery to the myocardium and reducing the incidence of occlusion. 
Click each tab below to learn more about different types of antiplatelet drugs. 
Aspirin
Aspirin is a nonsteroidal anti-inflammatory drug that inhibits platelet aggregation and is to manage many different conditions.
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Overview of the Drug
Prototype: aspirin
• Category: Nonsteroidal Anti-Inflammatory (NSAID) and Antiplatelet (Cyclooxygenase Inhibitor) 
• Primary Function: Used in the prevention of arterial thrombosis due to its antiplatelet effect. 
• Unique Features: Unique among NSAIDs for its ability to irreversibly inhibit platelet function, thereby reducing the risk of clot formation in arteries. 
Mechanism of Action
• Aspirin irreversibly inhibits the cyclooxygenase (COX) enzyme. This inhibition reduces the synthesis of thromboxane A2 (TXA2), a substance that promotes platelet aggregation. The action is irreversible for the lifespan of a platelet (7-10 days), which means new platelets have to be generated to regain normal platelet function. 
Indications and Therapeutic Uses
• Stroke and MI Prevention: Primary prevention of stroke or MI in individuals with risk factors like diabetes, hypertension, smoking, or hyperlipidemia. 
• During and After MI: Used for the reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction. The MONA (Morphine, Oxygen, Nitrates, Aspirin) protocol is commonly employed in acute cases to quickly address symptoms, prevent further cardiac damage, and reduce the risk of life-threatening complications.
• Preventing Stent Occlusion: In individuals with coronary stents, aspirin can be used to prevent stent thrombosis.
Off-Label Uses
• May be used for the prevention of colorectal cancer in some individuals with specific risk factors. 
• Employed in some rheumatologic diseases due to its anti-inflammatory properties. 
• May be used in small daily doses for its potential role in the prevention of Alzheimer’s disease, though this is not a widely endorsed use. 
Side Effects and Adverse Reactions
Side Effect Description
Hemorrhage The major complication from aspirin. This can occur anywhere in the body but many times can cause bleeding in the GI system.
Renal Impairment By inhibiting COX-1, aspirin can cause the kidneys to not have the prostaglandins needed for normal function, causing this.
Reye Syndrome Using aspirin in children under age 18 can cause this, manifested by encephalopathy and fatty liver.
Salicylism Symptoms include tinnitus, headache, and dizziness from supratherapeutic aspirin levels.
Precautions and Contraindications
Precautions
• Should be used carefully in clients taking anticoagulants like warfarin due to increased bleeding risk. 
• Should be avoided or used with caution in clients with a history of peptic ulcer disease or gastrointestinal bleeding. 
Contraindications 
• Contraindicated in clients with known aspirin allergy. 
• Contraindicated in children under age 18 due to the risk of Reye’s syndrome, particularly following viral infections. 
• Aspirin was previously classified as a Pregnancy Risk Category D agent with use contraindicated in clients unless the benefits outweigh the risks. It may cause anemia or postpartum hemorrhage.  
Drug Interactions
• Aspirin can interact with other NSAIDs like [ibuprofen, naproxen, and others], reducing its antiplatelet effect. 
• Aspirin can interact with anticoagulants (e.g., [warfarin, heparin, and other oral anticoagulants]), increasing the risk of bleeding. [Alcohol] use may also exacerbate the potential for GI bleeding. 
• Concurrent use of aspirin with [glucocorticoids] increases the risk of gastrointestinal ulceration.  
• Using aspirin concurrently with [ACE inhibitors or ARBs] can increase the risk of renal dysfunction. 
Dosing, Administration, & Client Teaching
Dosing
• Oral or rectal administration. 
• The dose and duration depend on the individual’s condition and risk factors. 
• Check drug dosing guidelines for individualized dosing. 
• Dose adjustment may be necessary in renal impairment. 
• For cardiovascular prophylaxis, low-dose aspirin (81-325 mg daily) is typically used. 
• Should be discontinued 5-7 days before any planned surgery due to bleeding risk. 
• It takes platelet function 10 days to return to normal after taking aspirin. 
• Not for use in pregnant or pediatric populations.  
Administration
• Oral or rectal administration. 
• Should be taken with food or a glass of water to minimize gastrointestinal discomfort. 
Client Teaching
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
• Clients should be advised about the signs of gastrointestinal bleeding, including black, tarry stools or blood in vomit. 
• Instruct clients on the importance of not taking additional NSAIDs to avoid increased risk of side effects. 
• Inform about the risk of increased bleeding during surgeries or dental procedures and the need to inform healthcare providers about aspirin use. 
Labs to Monitor
Basic Metabolic Panel (BMP)
• Assess kidney function if myopathy and rhabdomyolysis is suspected. 
Complete Blood Count (CBC)
• If signs of bleeding are present, a CBC may help to indicate the extent of blood loss. 
Serum Drug Levels
• Serum salicylate levels can be drawn to assess for aspirin toxicity or overdose. 
ADP Receptor Antagonists
Adenosine diphosphate (ADP) receptor antagonists are used in the management of thrombotic cardiovascular conditions by inhibiting platelet aggregation, particularly in preventing complications related to arterial thrombosis.
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Overview of the Drug
Prototype: clopidogrel (Plavix) 
• Category: P2Y12 Adenosine Diphosphate Receptor Antagonists 
• Primary Function: ADP receptor antagonists are antiplatelet drugs that prevent platelet aggregation by blocking the adenosine diphosphate (ADP) receptors on platelet surfaces. Clopidogrel and prasugrel cause irreversible receptor blockade, while ticagrelor causes reversible receptor blockade. 
• Unique Features: These drugs are crucial in preventing thrombotic events in arterial circulation.  
Mechanism of Action
• ADP receptor antagonists block the P2Y12 ADP receptor on the platelet surface, which plays a key role in platelet activation and aggregation. For most drugs in this category, this blockade is irreversible, persisting for the life of the platelet with platelet function returning to normal 7-10 days after the last dose. 
Indications and Therapeutic Uses
• During and After MI: Used for the reduction in the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction. The MONA (Morphine, Oxygen, Nitrates, Aspirin) protocol is commonly employed in acute cases to quickly address symptoms, prevent further cardiac damage, and reduce the risk of life-threatening complications. It is recommended to combine clopidogrel with aspirin in ACS. Clopidogrel can also be used in place of aspirin in clients with aspirin allergies.
• Preventing Stent Occlusion: In individuals with coronary stents, clopidogrel can be used to prevent stent thrombosis.
Side Effects and Adverse Reactions
Side Effect Description
Hemorrhage The major complication from clopidogrel. This can occur anywhere in the body but many times can cause bleeding in the GI system.
Thrombotic Thrombocytopenic Purpura (TTP) In the first two weeks of treatment, clients can develop this condition characterized by hemolytic anemia, neurologic symotoms, fever, and renal impairment. This is rare.
Precautions and Contraindications
Precautions
• Caution in clients with a history of bleeding disorders or those undergoing surgery. 
• Should be used carefully in clients taking anticoagulants like warfarin due to increased bleeding risk. 
• Should be avoided or used with caution in clients with a history of peptic ulcer disease or gastrointestinal bleeding. 
• Discontinue 5 days before surgery. 
Contraindications
• Contraindicated in clients with active pathological bleeding. 
Black Box Warning
• Clients with variant forms of the CYP2C19 gene can be poor metabolizers of clopidogrel and therefore may not convert it to its active form (which is required since it is a prodrug). This places them at risk for cardiovascular events. Genetic testing should be considered. 
Drug Interactions
• There is an increased bleeding risk when using ADP antagonists with other drugs that inhibit hemostasis, including [anticoagulants and antiplatelets]. 
• Certain drugs like [proton pump inhibitors] that are often prescribed with clopidogrel due to their ability to prevent gastric ulcers may reduce the effectiveness of some ADP receptor antagonists due to their inhibition of the CYP2C19 liver enzyme responsible for metabolizing clopidogrel. 
• Other drugs that inhibit the CYP2C19 enzyme, including [cimetidine, fluoxetine, fluconazole, ketoconazole], and others, may reduce the antiplatelet effects of clopidogrel. 
Dosing, Administration, & Client Teaching
Dosing
• Oral administration. 
• Check drug dosing guidelines for individualized dosing. 
• A loading dose may be used in acute settings followed by a maintenance dose. 
• Dosing can vary based on specific drug (e.g., clopidogrel, prasugrel). 
• It takes 10 days (the life span of a platelet) after discontinuing clopidogrel for platelet function to return to normal. 
• Clopidogrel is a prodrug that must be metabolized using the CYP2C19 enzyme. Some people may be poor metabolizers and providers should test for CYP2C19 variants as there are other drugs besides the prototype in this category. 
• May be used in place of aspirin for clients with aspirin allergies. 
Administration
• Oral administration. 
• A loading dose may be used in acute settings followed by a maintenance dose. 
Client Teaching
• Clients should be advised about the signs of gastrointestinal bleeding, including black, tarry stools or blood in vomit. 
• Instruct clients on the importance of not taking additional NSAIDs to avoid increased risk of side effects. 
• Inform about the risk of increased bleeding during surgeries or dental procedures and the need to inform healthcare providers about aspirin use. 
Labs to Monitor
Complete Blood Count (CBC)
• If signs of bleeding are present, a CBC may help to indicate the extent of blood loss. If there are concerns for TTP, platelet levels can also be assessed using the CBC. 
Beta-Blockers and Calcium Channel Blockers in Angina
Beta blockers and calcium channel blockers (CCBs) can be helpful in long-term management of angina. Beta blockers can be used for stable angina to enhance exercise tolerance by reducing heart rate and contractility. This decreases cardiac oxygen demand and a slower heart rate allows more thorough coronary artery perfusion during diastole to further improve myocardial oxygen supply. However, they are less effective for vasospastic angina. Conversely, CCBs, including verapamil, diltiazem, and nifedipine, are effective in stable and variant (Printzmetal) angina. They operate by dilating arterioles and reducing peripheral resistance to lower cardiac oxygen demand. Additionally, certain CCBs can relax coronary vasospasm, increasing oxygen supply to the heart. While effective, both drug classes require cautious administration considering potential adverse effects like bradycardia, bronchoconstriction, and reflex tachycardia (Rosenthal & Burchum, 2021). 
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Review the tables below for correct answers.

Question 1

Drug Action
Nitroglycerin Vasodilates arterioles and veins
Oxygen Enhances provision of a vital component of cellular metabolism to the myocardium
Morphine Narcotic for pain relief with vasodilatory properties
Aspirin Inhibits further platelet aggregation to help prevent vessel occlusion
Beta blockers Decrease the workload of the heart by decreasing heart rate and contractility
Calcium channel blockers Drug of choice for Variant/Printzmetal angina due to dilating and relaxing effect on coronary arteries. Two types: one that works only on blood vessels and the other works on the heart and blood vessels.

Question 2
 
Anticoagulants Qualities Antiplatelets
Examples: aspirin, clopidogrel x
x Reduces fibrin formation.
x Used for conditions that involve blood stasis.
Reduces the tendency of platelets to clump. x
Used for conditions that involve endothelial damage and platelets sticking to the injured site. x
x Examples: heparin, warfarin, dabigatran, apixaban, rivaroxaban
Management of Heart Disease 
There are many different types of cardiac conditions and most require a comprehensive approach to nonpharmacologic interventions and medication therapy using a combination of drug categories. Many different drugs can be used to treat the myriad of cardiac conditions impacting health and medication selection is influenced by the assessment of an individual’s overall health, comorbidities, and other specific health needs while minimizing side effects (Rosenthal & Burchum, 2021). 
Medications for Heart Failure 
Heart failure is one cardiac condition that may require specialized medications for treatment. Click each section below to learn more about medications that are indicated for heart failure. 
Loop Diuretics
Loop diuretics act on the ascending limb of the loop of Henle in the nephron to promote the excretion of sodium and water.
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Click through the activity below to learn more about loop diuretics, including dosing and administration guidelines (Rosenthal & Burchum, 2021). 
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Overview of the Drug
Prototype: furosemide (Lasix) 
• Category: Loop diuretic 
• Primary Function: Promotes extensive diuresis by inhibiting sodium and chloride reabsorption. 
• Unique Features: Effective across a range of kidney functions, including in renal impairment. Most powerful diuretic since it acts early in the nephron.
Mechanism of Action
• Loop diuretics block the Na-K-2Cl symporter in the ascending limb of the loop of Henle in the nephron, leading to increased excretion of sodium, chloride, potassium, and water. 
• The ascending loop of Henle is where 20% of filtered sodium and chloride is reabsorbed into the blood. By blocking that process, loop diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of water, causing water and solutes to be retained in the nephron and promoting excretion. 
• Can lead to significant diuresis, quickly reducing fluid volume. 
Indications and Therapeutic Uses
• Various Forms of Edema: Helps promote diuresis in conditions that create edema (heart failure, cirrhosis, renal disease, hypertension, etc.).
• Hypertension: Used when a strong diuretic effect is desired, not routinely. Also used for hypertension clients with low GFR (since thiazides won’t work in kidney impairment).
• Heart Failure: Rapidly reduces fluid accumulation to reduce the workload of the heart.
• Pulmonary Edema: Reduces fluid congestion in the vasculature and helps promote diuresis.
• Acute Kidney Injury: Helps maintain urine output. 
Side Effects and Adverse Reactions
Side Effect Description
Hypokalemia An electrolyte imbalance where there is too little potassium. In loop diuretics, clients can also experience low magnesium levels.
Hyponatremia An electrolyte imbalance where there is too little sodium. In loop diuretics, clients can also experience low chlorine levels.
Hypovolemia Decreased blood volume and dehydration from excessive diuresis.
Hypotension Low blood pressure. Orthostatic blood pressure changes can also occur.
Pre-renal acute kidney injury From decreased kidney perfusion related to low blood volume.
Ototoxicity Toxicity related to the ear which can cause ringing in the ears and hearing loss. Worse when used with other ototoxic drugs (like aminoglycosides).
Hyperglycemia High blood sugar. Diabetic clients should use caution.
Hyperuricemia High uric acid levels. Clients with gout should use caution.
Other Pancreatitis, jaundice, rash.
Precautions and Contraindications
Precautions
• Use with caution in clients with severe electrolyte imbalances. 
• Risks in clients with pre-existing hypotension or at risk for falls. 
• Potential for acute kidney injury in cases of severe dehydration. 
Contraindications
• Contraindicated for clients with sulfa allergy. 
• Considerations in pregnant or breastfeeding clients. 
• May decrease breast milk production through excessive diuresis. 
• Only use in pregnancy if absolutely necessary due to risks. 
Black Box Warning
• May result in profound diuresis and dosing is individualized with medical supervision required.
Drug Interactions
• Elevated risk of [ototoxicity] with aminoglycoside antibiotics. 
• Potentiation of other antihypertensive drugs, leading to [hypotension]. 
• The potential for drugs like digoxin and lithium to accumulate and cause toxicity due to [hypokalemia and hyponatremia]. 
• [non-steroidal anti-inflammatory drugs (NSAIDs)] can reduce the diuretic effect. 
Dosing, Administration, & Client Teaching
Dosing
• Dosing varies based on the condition, severity, and client response. 
• Check drug dosing guidelines for individualized dosing. 
• Typically taken once or twice per day. 
• Consider the need for a potassium supplement or another drug with potassium-sparing qualities (e.g., potassium-sparing diuretics) to counter hypokalemia. 
Administration
• Administered orally, intravenously, or intramuscularly. 
• IV administration in acute settings, requiring slow administration to avoid rapid electrolyte shifts. 
Client Teaching
• Administered orally, intravenously, or intramuscularly. 
• IV administration in acute settings, requiring slow administration to avoid rapid electrolyte shifts. 
Labs to Monitor
Basic Metabolic Panel (BMP)
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
• Blood glucose levels in diabetic clients. 
Serum Drug Levels
• Serum drug levels for lithium or digoxin, if applicable. 
Neprilysin Inhibitors
Neprilysin inhibitors enhance the levels of natriuretic peptides to promote diuresis, vasodilation, and natriuresis.
Learn More
Click through the activity below to learn more about angiotensin receptor neprilysin inhibitors (ARNIs), including dosing and administration guidelines (Rosenthal & Burchum, 2021). 
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Overview of the Drug
Prototype: sacubitril/valsartan (Entresto) 
• Category: Angiotensin Receptor Neprilysin Inhibitor (ARNI) 
• Primary Function: Neprilysin is an enzyme that breaks down natriuretic peptides. Inhibition of neprilysin increases levels of natriuretic peptides, leading to natriuresis, diuresis, and vasodilation. 
• Unique Features: ARNIs are a novel class of cardiovascular drugs. They combine the mechanisms of angiotensin receptor blockers (ARBs) and neprilysin inhibitors. 
Mechanism of Action
• Sacubitril/valsartan operates by increasing neprilysin, an enzyme that breaks down natriuretic peptides, while simultaneously reducing the adverse effects of the renin-angiotensin-aldosterone system (RAAS) by blocking the action of angiotensin II at receptor sites. Natriuretic peptides like ANP and BNP regulate fluid balance. Inhibition of neprilysin increases levels of natriuretic peptides, leading to natriuresis, diuresis, and vasodilation, aiding in reducing fluid overload and decreasing the heart’s workload. 
Indications and Therapeutic Uses
• Heart Failure: Specifically indicated for New York Heart Association (NYHA) Class II-IV heart failure or pediatric heart failure in clients over one year old. Studies have demonstrated a mortality benefit in heart failure patients using ARNIs. Used as a replacement for ACE inhibitors or ARBs in certain clients. 
Side Effects and Adverse Reactions
Side Effect Description
Hyperkalemia An electrolyte imbalance where there is too much potassium. This risk is increased when used with other drugs or salt substitutes that can increase potassium. This side effect can cause cardiac arrhythmias or death.
Renal Failure In clients with renal artery stenosis or only one kidney, ARBs can cause this.
Angioedema Potentially fatal reaction from increased capillary permeability and edema of the tongue, mouth, or face. This can be life threatening due to airway obstruction. Lower risk than in ACE inhibitors.
Precautions and Contraindications
Precautions
• Caution in clients with renal impairment or hyperkalemia. 
• Do not use simultaneously with ACE Inhibitors, ARBs, in clients with liver disease or a history of angioedema. 
Contraindications
• Not recommended for use in clients with a history of angioedema. 
• Contraindicated in pregnant clients. 
Black Box Warning
• Fetal toxicity resulting in injury or death. 
Drug Interactions
• Drug interactions with other drugs affecting the RAAS that also decrease fluid volume and increase potassium, including [ACE inhibitors, ARBs, and potassium-sparing diuretics]. 
Dosing, Administration, & Client Teaching
Dosing
• Oral dosing. 
• Dose adjustment may be necessary in renal impairment. 
• Check drug dosing guidelines for individualized dosing. 
• Start dose low to avoid hypotension. 
• Allow 36-hour washout period when switching to ARNIs from other drugs affecting the RAAS. 
Administration
• Oral administration. 
Client Teaching
• Dietary advice, particularly on potassium-rich foods. 
• Awareness of potential blood pressure changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Advise to report any signs of facial swelling, difficulty breathing (angioedema), persistent cough, or significant changes in urine output. 
• Monitor blood pressure regularly, especially after initiating therapy. 
• Advise pregnant clients or those planning pregnancy to discuss medication alternatives with their healthcare provider. 
Labs to Monitor
Basic Metabolic Panel
• Regular monitoring of electrolytes, especially potassium. 
• Assessing renal function, including creatinine and BUN levels. 
Cardiac Glycosides
While most other medication categories covered this week are first- and second-line choices for managing heart disease, cardiac glycosides are reserved for clients with conditions that other medications have failed to adequately manage. Cardiac glycosides increase the force of cardiac muscle contractions and slow the heart rate and are used in heart failure and certain arrhythmias.
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Click through the activity below to learn more about cardiac glycosides, including dosing and administration guidelines (Rosenthal & Burchum, 2021). 
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Overview of the Drug
Prototype: digoxin (Lanoxin) 
• Category: Cardiac Glycosides 
• Primary Function: Digoxin is used primarily in the treatment of heart failure and certain cardiac arrhythmias when other drugs have not been effective. 
• Unique Features: The use of digoxin is no longer a first line drug for treating heart failure since other drugs (ACEs, ARBs, beta-blockers, CCBs) are safer and more effective. In the U.S., digoxin is the only cardiac glycoside available. 
Mechanism of Action
• Digoxin increases myocardial contractility (positive inotropic effect) by inhibiting an enzyme called the sodium, potassium-adenosine triphosphatase (Na+, K+-ATPase). This promotes calcium accumulation in myocytes that increases the force of contraction. Potassium competes with digoxin for binding to the Na+, K+-ATPase enzyme, meaning that in hypokalemia there is excessive binding of digoxin and inhibition of the Na+, K+-ATPase, resulting in digoxin toxicity. This means that maintaining a normal potassium level is critical for clients receiving digoxin therapy. 
• The increased contractility from digoxin increases cardiac output resulting in increased perfusion to organs, including the kidney. This means that urine production increases, renin release declines, and sympathetic tone decreases. This decrease in sympathetic tone reduces heart rate allowing increased time for ventricular filling, decreased afterload, and decreased myocardial workload. 
• Digoxin also reduces the conductivity of the heart’s electrical impulses through the SA node, AV node, and Purkinje fibers. This makes digoxin useful for treating arrhythmias. 
Indications and Therapeutic Uses
• Heart Failure: Digoxin helps increase contractility in clients with HFrEF, helping improve symptoms, exercise tolerance, and quality of life in heart failure clients.
• Arrhythmias: Decreasing conductivity through the SA node, AV node, and Purkinje fibers in the heart decreases heart rate and conductivity to manage arrhythmias, mainly atrial fibrillation. This same mechanism can also cause arrhythmias.
Side Effects and Adverse Reactions
Side Effect Description
Arrhythmias Clients are prone to developing ventricular arrhythmias, particularly those with hypokalemia.
GI Disturbances Nausea, vomiting, and loss of appetite. This can indicate toxicity.
Bradycardia or Heart Block Clients can experience low heart rate and various blockages of impulse conduction.
Visual Disturbances Clients can experience a yellow tinge to their vision or see halos around things. This can indicate toxicity.
Fatigue Clients can become tired.
Precautions and Contraindications
Precautions
• Use with caution in clients with renal impairment, hypokalemia, or existing AV block. 
• Narrow therapeutic index with toxicity occurring in levels only slightly above therapeutic. 
Contraindications
• Contraindicated in clients with ventricular fibrillation. 
Black Box Warning
• Excessive use can worsen arrhythmias or lead to new arrhythmias. 
Drug Interactions
• [Thiazide and loop diuretics] can increase potassium loss, causing hypokalemia. This can cause digoxin toxicity. 
• [Beta-blockers and calcium channel blockers (non-dihydropyridines)] can also decrease contractility and heart rate, potentially causing excessive cardiosuppression when combined with digoxin. 
• Certain drugs can decrease digoxin levels by decreasing absorption, including [cholestyramine, metoclopramide] and others. 
• Drugs that increase digoxin levels by increasing absorption include [antacids, aminoglycosides, azithromycin, omeprazole], and others. 
• Drugs can increase digoxin levels by decreasing excretion or altering distribution, including [alprazolam, amiodarone, atorvastatin, captopril, calcium channel blockers], and others. 
Dosing, Administration, & Client Teaching
Dosing
• Available in PO tablets, elixir, and IV solution. 
• Check drug dosing guidelines for individualized dosing. 
• Consider the need for a potassium supplement or another drug with potassium-sparing qualities (e.g., potassium-sparing diuretics) to counter hypokalemia if present. 
• Dose adjustment may be necessary in renal impairment. 
• DigiBind and DigiFab are IgG antidigoxin antibodies that bind free digoxin in the blood and are treatments for digoxin overdose. 
• Monitor serum digoxin levels with goal for therapeutic range 0.5-0.8 ng/mL. There is no therapeutic result over 1 ng/mL and toxicity occurs above 2 ng/mL. 
• Loading doses are no longer typically used. 
Administration
• Oral or IV administration. 
• Assess baseline heart rate for one minute (hold if pulse is below 60 bpm). Optimal assessment includes auscultation of apical heart rate. 
• DigiBind and DigiFab are IgG antidigoxin antibodies that bind free digoxin in the blood and are treatments for digoxin overdose. 
Client Teaching
• Importance of monitoring for signs of dehydration and electrolyte imbalance. 
• Dietary advice, particularly on potassium-rich foods. 
• Awareness of potential heart rate and rhythm changes and risk of dizziness or falls. 
• Educate about the importance of adherence and not stopping abruptly. 
• Teach the importance of regular monitoring of heart rate for one minute (hold if pulse is below 60 bpm). 
• Teach clients to recognize signs of toxicity and hypokalemia. 
Labs to Monitor
Basic Metabolic Panel (BMP)
• Monitor electrolytes, particularly potassium, due to risk of hypokalemia-induced toxicity. 
• Monitor renal function tests due to renal excretion of the drug. 
Serum Drug Levels
• Regular monitoring of serum digoxin levels is required (narrow therapeutic range: 0.5-0.8 ng/mL, up to 2.0 until toxicity). 
Learn By Applying
Apply what you have learned to the clinical scenarios below. 
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Learn By Applying Transcript
Question 1
Drug Action
Furosemide (Lasix) Most powerful diuretic. Known to cause electrolyte imbalances. Can cause ototoxicity. Does not require adequate kidney function to work.
HCTZ Requires adequate kidney function to work. Can be useful with osteoporosis due to effects on calcium reabsorption. Can also cause electrolyte disturbances.
Spironolactone (Aldactone) Produces scant diuresis. Used for potassium sparing effects. Has endocrine side effects.
Triamterene (Dyrenium) Produces scant diuresis. Used for potassium sparing properties but no endocrine side effects.
Question 2
The NP is performing an assessment of current medications for Lila Potter, a 67-year-old female. Lila is taking the following medications: furosemide (Lasix), spironolactone (Aldactone), and Klor-Con. Which of the following is the priority concern related to these medications being taken together? 
• Hypokalemia 
• Hyperkalemia (Correct answer)
• Hypernatremia 
• Hyponatremia 
Rationale: When combining spironolactone with potassium supplements, like Klor-Con, hyperkalemia can occur. Hypokalemia, hypernatremia, and hyponatremia are not risks from combining these medications. 
 
Question 3
Many clients with heart failure take furosemide (Lasix) and digoxin (Lanoxin) simultaneously. The NP knows to monitor for electrolyte abnormalities, particularly ____________, associated with taking these medications simultaneously since that can lead to digoxin toxicity. 
Correct answer: Hypokalemia 
Rationale: Furosemide can cause hypokalemia. When combined with digoxin, hypokalemia can cause digoxin toxicity. 
 
Question 4
A client is currently taking aminoglycosides for a urinary tract infection and requires a prescription for a diuretic. The NP knows that ________ diuretics are not appropriate in clients taking aminoglycosides due to an increased risk of ototoxicity. 
Correct answer: Loop 
Rationale: Loop diuretics can cause ototoxicity, especially when combined with other drugs that cause ototoxicity, such as aminoglycosides. 
 
Question 5
The NP checks the client’s most recent digoxin level. It is 2.8. Which of the following is the priority action take? 
• Order potassium 
• Order DigiFab (digoxin immune fab) (Correct answer)
• Order kayexalate 
• This is normal and nothing needs to be done 
Rationale: Therapeutic levels of digoxin are between 0.5-0.8, with 2 as the threshold for toxicity to develop. A digoxin level above 2 necessitates immediate action, and administration of DigiFab is indicated. Since the potassium level is unknown, there is no way to determine if potassium supplementation is required at this time, although digoxin toxicity can occur in the presence of hypokalemia. Kayexelate is ordered for hyperkalemia.  
 
Question 6
Nikisha Fogo is an 82-year-old female taking digoxin (Lanoxin), furosemide (Lasix), and spironolactone (Aldactone). Which of the following statements require intervention by the NP? Select all that apply. 
• “I weigh myself every day and keep a log” 
• “I check my pulse for 30 seconds before administering my medication” (Correct answer)
• “I monitor myself for weakness” 
• “I eat bran muffins with my medications so I don’t get an upset stomach” (Correct answer)
• “I keep my appointments to get my lab work checked” 
Rationale: Clients taking digoxin should assess their heart rate for a full minute prior to medication administration and avoid bran muffins as bran decreases digoxin absorption. Clients should weigh themselves daily, monitor themselves for weakness (a sign of hypokalemia), and keep their laboratory appointments. 

Lifespan Considerations 
Click each plus (+) sign in the activity below to learn more about lifespan considerations for pharmacologic management of chronic coronary conditions (Rosenthal & Burchum, 2021). 
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Lifespan Considerations Transcript 
Pregnant and Breastfeeding Clients
• In 2015, the FDA revised pregnancy labeling guidelines to move away from the A, B, C, D, and X labels to the Pregnancy and Lactation Labeling Rule (PLLR), which requires labels to a summary of the risk of using the drug during pregnancy and lactation, data supporting the summary, and counseling information. These labels must be updated when new information is available. Although the PLLR is recommended, original labeling categories are often referenced in practice and across settings and, therefore, provided in this course.
• Consider the safety of drugs for chronic coronary disease for pregnant and breastfeeding clients. 
• What pregnancy category is the drug? 
• Highly lipid-soluble drugs cross membranes and may enter breastmilk. 
• Antiplatelets can increase the risk of bleeding around the placenta and therefore the health of the client and fetus. 
• Consider altered pharmacokinetics related to pregnancy. 
Pediatric Clients
• Coronary conditions are rare in pediatric populations. 
• Consider the ability of the family to manage a medication regimen. 
• Consider altered pharmacokinetics based on age. 
Older Adults
• Consider the risk for altered myocardial perfusion related to coronary ischemia in older adults.  
• Falls can place older adults at a higher risk of bleeding (in the brain and other areas) when on antiplatelets. 
• Consider the ability of the client and support system to safely self-administer medications without skipping or doubling doses. 
• Consider how lifestyle modifications may be necessary in addition to pharmacologic interventions.  
• Consider altered pharmacokinetics based on age-related changes. 
• Consider polypharmacy and drug interactions. 

Clinical Practice Guidelines for Chronic Coronary Disease 
CPGs for chronic coronary disease offer evidence-based recommendations for diagnosing and managing this condition, emphasizing risk factor modification, lifestyle interventions, and appropriate medication therapy to reduce cardiovascular events and improve outcomes.  
Learn By Applying 
Apply what you have learned to the clinical scenarios below. Each client has an appointment to discuss issues related to the management of their hypertension. Select the most appropriate management plan for each client using the Clinical Practice Guidelines for chronic coronary disease and your textbook for drug names and dosages.
Client One: Peter Xi
Examine the image below to learn more about the client to help you write an appropriate and individualized prescription. 

Peter Xi Image Description
Peter Xi, a 55-year-old male (DOB: 1/25/1969) presents to the clinic today for a follow-up appointment three months after beginning statin therapy for high cholesterol. His lab results demonstrate persistent high cholesterol levels (particularly LDL levels which are > 190mg/dL), elevated creatine kinase (CK), and elevated liver function tests. Renal function is normal. The client complains of slight RUQ discomfort and muscle aches with the physical exam otherwise normal. 
Past Medical History: High Cholesterol, Stable Angina, MI 11 months ago 
Allergies: Aspirin
Medications: rosuvastatin (Crestor) 20mg PO daily, metoprolol (Lopressor) 50mg PO BID, aspirin 81mg PO daily 
Social History: The client does not drink alcohol and has never smoked cigarettes. 
Physical Exam:  
• Height: 5 ft 8 in
• Weight: 175 lbs
• Body Mass Index (BMI):  26.6
• Blood Pressure (BP): 124/71
• Heart Rate (HR): 82
• Respiratory Rate (RR): 17 
• Oxygen Saturation (O2SAT): 96% on RA
• Temperature (TEMP): 98.6 oral
Write an appropriate prescription for this client in the activity below. Click the “Show Answers” option that will appear once all fields are complete to compare your response with the correct answer.

Client Prescription Transcript
An appropriate prescription for Peter is:
Client Name:  Peter Xi 
Date of Birth: 1/25/1969 
Date Prescribed: Current Date 
Medication Name and Strength:  atorvastatin (Lipitor) 40mg 
Quantity:  30 
Directions: Take one 40mg tablet by mouth daily at bedtime 
Refills (0-4): 3 
Dispense as Written: 
Generic Substitution Permitted: 
• Either Dispense as Written or Generic Substitution Permitted should be checked on every written prescription depending on what is best for each client.  Refer to the week 1 lesson for criteria.  
Rationale: According to the CPG, this client requires high-intensity statin therapy. Originally, the client was started on rosuvastatin and after several months, there was no reduction in cholesterol levels and signs of toxicity developed. This caused the NP to suspect that this client has pharmacogenetic alterations in metabolism related to his Asian heritage, as rosuvastatin, in particular, can cause toxicity in Asian populations (Rosenthal & Burchum, 2021). According to the CPG, the client requires high-intensity statin therapy and atorvastatin is indicated. The client should have 3 refills as a re-evaluation is indicated between 4 and 12 weeks (Viriani et al., 2023). 
 Client Two: Tyrone Ball
Examine the image below to learn more about the client to help you write an appropriate and individualized prescription. 

Tyrone Ball Image Description
Tyrone Ball,  a 72-year-old male (DOB: 2/7/1952) presents to the clinic today one day after discharge from the hospital following PCI with stent placement x 2 for a STEMI. Labs from his inpatient stay reveal that his cholesterol is adequately controlled and are otherwise normal. His physical exam reveals the PCI insertion site on the right groin looks normal and does not have any bleeding or hematoma.
Past Medical History:  TIA, High Cholesterol, Hypertension 
Allergies: Aspirin
Medications: atorvastatin (Lipitor) 40mg PO daily and diltiazem (Cardizem) 120mg PO BID 
Social History: The client quit smoking last year and has alcohol only at special occasions, estimating the occurrence at twice per year. 
Physical Exam:  
• Height: 5 ft 11 in
• Weight: 205 lbs
• Body Mass Index (BMI): 28.6
• Blood Pressure (BP): 121/69
• Heart Rate (HR): 87
• Respiratory Rate (RR): 19 
• Oxygen Saturation (O2SAT): 98% on RA
• Temperature (TEMP): 98.6 oral
Write an appropriate prescription for this client in the activity below. Click the “Show Answers” option that will appear once all fields are complete to compare your response with the correct answer.
 

Patient Prescription Transcript
An appropriate prescription for Tyrone is:
Client Name:  Tyrone Ball 
Date of Birth: 2/7/1952 
Date Prescribed: Current Date 
Medication Name and Strength:  clopidogrel (Plavix) 75mg 
Quantity:  30 
Directions: Take one 75mg tablet by mouth daily 
Refills (0-4): 2 
Dispense as Written: 
Generic Substitution Permitted: 
• Either Dispense as Written or Generic Substitution Permitted should be checked on every written prescription depending on what is best for each client.  Refer to the week 1 lesson for criteria.  
Rationale: While the CPG recommends dual antiplatelet therapy (DAPT) with aspirin and ADP receptor antagonists, the client is allergic to aspirin. Clopidogrel is therefore the antiplatelet drug of choice to prevent stent occlusion. The NP could also consider adding a DOAC, as that may be indicated from recent studies, according to the CPG (Viriani et al., 2023). Two refills are provided as the provider should follow up with the client within two months to assess for any adverse reactions. 

References
Joglar, J.A., Chung, M.K., Armbruster, A.L., Benjamin, E.J., Chyou, J.Y., Cronin, E.M., Deswal, A., Eckhardt, L.L., Goldberger, Z.D., Gopinathannair, R., Gorenek, B., Hess, P.L., Hlatky, M., Hogan, G., Ibeh, C., Indik, J.H., Kido, K., Kusumoto, F., Link, M.S., Linta, K.T., Marcus, G.M., McCarthy, P.M., Patel, N., Patton, K.K., Perez, M.V., Piccini, J.P., Russo, A.M., Sanders, P., Streur, M.M., Thomas, K.L., Times, S., Tisdale, J.E., Valente, A.M., & Van Wagoner, D.R. (2024). 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: A report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. Circulation, 149, e1-e156. https://doi.org/10.1161/CIR.0000000000001193  
Luu, B., Kayingo, G., & Hass, V.M. (2021). Advanced pharmacology for prescribers. Springer Publishing LLC. 
Rosenthal, L., & Burchum, J. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.). Elsevier. 
Whelton, P.K., Carey, R.M., Aronow, W.S., Casey, D.E., Collins, K.J., Himmelfarb, C.D., DePalma, S.M., Gidding, S., Jones, D.W., MacLaughlin, E.J., Muntner, P., Ovbiagele, B., Smith, S.C., Spencer, C.C., Stafford, R.S., Taler, S.J., Thomas, R.J., Williams, K.A., Williamson, J.D., & Wright, J.T. (2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Journal of the American College of Cardiology, 71(19), e127-e248. https://doi.org/10.1016/j.jacc.2017.11.006  
Viriani, S.S., Newby, L.K., Arnold, S.V., Bittner, V., Brewer, L.C., Demeter, S.H., Dixon, D.L., Fearon, W.F., Hess, B., Johnson, H.M., Kazi, D.S., Kolte, D., Kumbhani, D.J., LoFaso, J., Mahtta, S., Mark, D.B., Minissian, M., Navar, A.M., Patel, A.R., Piano, M.R., Rodriguez, F., Talbot, A.W., Taqueti, V.R., Thomas, R.J., van Diepen, S., Wiggins, B., & Williams, M.S. (2023). 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA guideline for the management of patients with chronic coronary disease: A report of the American Heart Association/American College of Cardiology joint committee on clinical practice guidelines. Circulation, 148, e9-e119. https://doi.org/10.1161/CIR.0000000000001168  

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