LESSON 1: PHARMACOLOGY NCM 106

SEMESTER 1 | ACADEMIC YEAR 2024-2025|MIDTERMS

CARDIOVASCULAR AGENTS

● Cardiovascular System Components: Heart, blood

vessels (arteries, veins), blood flow.
● Oxygenated Blood: Flows through arteries →
arterioles → capillaries.
● Capillary Function: Delivers nutrients and absorbs
waste (CO2, urea, creatinine, ammonia).
● Deoxygenated Blood: Returns via venules and veins
to be processed by lungs and kidneys.
● Heart's Role: Pumps blood, providing energy for
circulation.
● Blockages: Can impede blood flow.

CONDUCTION OF ELECTRICAL IMPULSE

❖ Myocardium Function: Generates and conducts

electrical impulses.
❖ Sinoatrial (SA) Node: Primary pacemaker, located in
the right atrium, regulates heartbeat (60-80
beats/min).
❖ Atrioventricular (AV) Node: Secondary pacemaker,
located in interatrial septum, fires at 40-60
beats/min. If the SA node fails, AV node takes over,
resulting in a slower heart rate.
CARDIOVASCULAR AGENTS ❖ Bundle of His: Continuous tract of fibers from the AV
node that sends impulses to ventricles.
➔ Heart Structure: Four chambers (right atrium, left ❖ Independent Contraction: Ventricles can contract at
atrium, right ventricle, left ventricle). 30-40 beats/min without node influence.
➔ Blood Flow: Right atrium → deoxygenated blood; ❖ Influencing Drugs: Calcium, digitalis, and quinidine
right ventricle → pumps to lungs; left atrium → affect cardiac contraction.
oxygenated blood; left ventricle → pumps to aorta ❖ Nervous System Impact: Sympathetic system
for systemic circulation. increases heart rate; parasympathetic system
➔ Myocardium: Thick-walled muscle, especially in decreases heart rate.
ventricles, generates pumping force.
➔ Atria: Thin-walled, less muscular, receives blood. REGULATION OF HEART RATE
➔ Protective Layers: Pericardium (outer covering), AND BLOOD FLOW
endocardium (inner lining, three layers).
➔ Valves: Four total (tricuspid, mitral, pulmonic, aortic) ➢ Heart Rate: Beats 60-80 times/min in adults,
control blood flow. pumping blood into systemic circulation.
➔ Coronary Arteries: Right and left arteries supply ➢ Blood Pressure: Average systemic arterial pressure is
blood to heart; blockages can cause myocardial 120/80 mm Hg, determined by peripheral resistance
infarction (heart attack). and cardiac output.
➢ Cardiac Output: Volume of blood expelled in 1
minute; average is 4-8 L/min (calculated by heart
rate × stroke volume).

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➢ Stroke Volume: Amount ejected from left ventricle Systemic Circulation:

per heartbeat, approximately 70 mL/beat.
➢ Factors Influencing Stroke Volume: ● Heart pumps blood from the left ventricle to the
❖ Preload: Blood flow force stretching the aorta and into general circulation.
ventricle; increased preload can raise stroke ● Arteries and arterioles deliver blood to capillary
volume, while decreased preload can lower beds.
it. ● Nutrients are exchanged for waste products in
❖ Contractility: Force of ventricular capillaries.
contraction. ● Blood returns to the heart through venules and
❖ Afterload: Resistance to blood ejection; veins.
increased afterload decreases stroke
volume, while decreased afterload BLOOD
increases it.
➢ Drug Influence: Specific drugs can modify preload ● Blood Composition: Plasma (55% of total blood
and afterload, affecting stroke volume and cardiac volume), red blood cells (RBCs), white blood cells
output. Vasodilators typically decrease both, (WBCs), and platelets.
lowering arterial pressure and cardiac output. ● Plasma: 90% water, 10% solutes (glucose, proteins,
lipids, amino acids, electrolytes, hormones, gasses).
● Functions of Blood: Provides nutrients and oxygen
to body cells; oxygen mainly carried by hemoglobin
in RBCs.
● White Blood Cells: Major defense mechanism;
engulf microorganisms and produce antibodies.
● Platelets: Facilitate blood coagulation.
● Cell Lifespan: RBCs ~120 days; WBCs 2-24 hours.

CARDIAC GLYCOSIDES, ANTIANGINALS,

AND ANTIDYSRHYTHMICS

Drug Groups: Three groups discussed—cardiac glycosides,

antianginals, and antidysrhythmics.

Functions:

● Cardiac Glycosides: Regulate heart contraction.

● Antianginals: Manage blood flow to the myocardium
CIRCULATION (heart muscle).
● Antidysrhythmics: Control heart rate and rhythm.
Types of Circulation: Two types—pulmonary and systemic.
Pulmonary Circulation: CARDIAC GLYCOSIDES

● Heart pumps deoxygenated blood from the right ★ Historical Use: Digitalis used since 1200 AD; one of
ventricle to lungs via pulmonary artery. the oldest drugs.
● Blood in the pulmonary artery has high carbon ★ Source: Obtained from purple and white foxglove
dioxide concentration. plant; can be poisonous.
● Oxygenated blood returns to the left atrium via ★ Early Use: In 1785, William Withering used it to treat
pulmonary vein. “dropsy” (edema) without realizing it was due to
heart failure.

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★ Current Use: Effective for treating heart failure (HF), HF Staging:

also known as cardiac failure (CF) or congestive
heart failure (CHF). ● In 2001, ACC and AHA classified heart failure (HF) in
★ Heart Failure Description: Occurs when weakened stages based on severity.
myocardium loses ability to pump blood, leading to ● Early stage: No symptoms and no structural heart
systemic circulation issues. damage.
★ CHF Condition: Results from failed compensatory
mechanisms, causing congestion in peripheral and Further Information: Detailed staging information available
lung tissues. at [Link]/about-heart-failure/[Link].
★ Causes of HF: Includes chronic hypertension,
myocardial infarction (MI), coronary artery disease
(CAD), valvular heart disease, congenital heart
disease, and arteriosclerosis.

Types of Heart Failure: Left-sided and right-sided.

Left-Sided Heart Failure:

➔ Occurs when the left ventricle fails to pump blood

effectively into the aorta.
➔ Causes blood to back up into lung tissue, leading to
shortness of breath (SOB) and dyspnea.

Right-Sided Heart Failure:

➔ Occurs when the heart fails to pump blood from the

right atrium effectively.
➔ Results in blood backing up into peripheral tissues, ● Cardiac Glycosides: Naturally occurring in plants like
causing peripheral edema. Digitalis; also known as digitalis glycosides.
● Mechanism of Action: Inhibit sodium-potassium
Interdependence: Left-sided failure can lead to right-sided pump, increasing intracellular sodium, which leads
failure and vice versa. to calcium influx and improved cardiac muscle
contraction.
Myocardial Hypertrophy: Can lead to cardiomegaly (enlarged ● Effects on Heart Muscle:
heart), a major issue associated with progressive heart 1. Positive Inotropic Action: Increases
failure. myocardial contraction and stroke volume.
2. Negative Chronotropic Action: Decreases
heart rate.
Increased Preload: 3. Negative Dromotropic Action: Decreases
conduction of heart cells.
● Results from excess blood volume in the ventricle at ● Overall Benefits: Enhances cardiac output,
the end of diastole. decreases preload, improves blood flow to periphery
● Caused by pathological thickening and stretching of and kidneys, reduces edema, and promotes fluid
ventricular walls, leading to greater filling pressure excretion, thereby decreasing fluid retention in lungs
in a weakened heart. and extremities.
● Digoxin: Increases force and velocity of myocardial
Increased Afterload: contraction but does not prolong life.

● Additional pressure in the ventricular wall due to

excess resistance in the aorta.
● Resistance must be overcome to open the aortic Digoxin: Secondary drug for heart failure (HF).
valve for blood ejection into circulation.

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First-Line Drugs for Acute HF: ● Obesity: Should be addressed, as it can increase
cardiovascular issues; patients should modify
● Intravenous Inotropic Agents: Dopamine and unhealthy behaviors.
dobutamine.
● Phosphodiesterase Inhibitors: Milrinone. LABORATORY TESTS

Other HF Medications: Atrial Natriuretic Hormone (ANH/ANP):

● Oral diuretics, beta blockers, ACE inhibitors, ● Reference value: 20 to 77 pg/mL (20 to 77 ng/L SI
angiotensin-receptor blockers (ARBs), calcium units).
channel blockers, and vasodilators. ● Elevated levels may confirm heart failure (HF).
● Oral administration allows patients to manage ● Secreted from heart atria, acts as an antagonist to
treatment at home. renin and aldosterone.
● Released during atrial expansion; produces
Cardiac Glycosides in Dysrhythmias: vasodilation and increases glomerular filtration rate.
● Results in increased urine volume, decreasing blood
● Used to correct atrial fibrillation (rapid volume and pressure.
uncoordinated contractions) and atrial flutter
(200-300 beats/min). Brain Natriuretic Peptide (BNP):
● Effects: Negative chronotropic (decreases heart rate)
and negative dromotropic (decreases conduction ● Reference values: Desired <100 pg/mL; positive
through AV node). >100 pg/mL.
● Primarily secreted from atrial cardiac cells; aids in
Management of Atrial Fibrillation: diagnosing HF.
● Elevated BNP helps differentiate dyspnea due to HF
● If digoxin fails, the goal is to slow heart rate by from lung dysfunction.
reducing electrical impulses through the AV node. ● BNP often >100 pg/mL in women 65+; can be 160
● Calcium Channel Blocker: Verapamil (Calan) may be pg/mL in an 80-year-old woman; markedly higher
prescribed. (e.g., 400 pg/mL) in HF.
● Thromboembolism Prevention: Warfarin ● BNP is more sensitive than ANP for diagnosing HF; a
(Coumadin) prescribed concurrently to prevent bedside machine is available for testing.
clots; discussed in Chapter 45.

NONPHARMACOLOGIC MEASURES
TO TREAT HEART FAILURE

Non Drug Therapy: Essential for managing heart failure (HF).

Do Not Confuse:
General Recommendations:
● Digoxin (Lanoxin) vs. Digitoxin: Both are cardiac
glycosides.
● Salt Intake: Limit to 2 g/day (approximately 1
● Digoxin: First-choice drug; half-life is 36 hours.
teaspoon).
● Digitoxin: Rarely prescribed; half-life is 4 to 9
● Alcohol Intake: Decrease to 1 drink per day or avoid
days; not available in the United States.
completely to prevent cardiomyopathy.
● Fluid Intake: May be restricted, especially in severe
conditions.
● Smoking: Should be avoided as it deprives the heart
of oxygen.
● Exercise: Mild activities like walking or biking are
recommended.

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DIGOXIN ● Headaches, malaise, blurred vision, visual illusions

(halos).
Pharmacokinetics of Digoxin ● Confusion and delirium.
● Older adults are at higher risk.
● Absorption:
○ Oral tablets: 70% Cardiotoxicity: Serious adverse reaction leading to ventricular
○ Liquid/capsule: 90% dysrhythmias.
● Protein Binding: 30%
● Half-Life: 30 to 40 hours (risk of accumulation and Contributing Factors:
digitalis toxicity).
● Monitoring: 1. Suppression of AV conduction.
○ Serum levels are drawn when digitalis 2. Increased automaticity.
toxicity is suspected to assess extent and 3. Decreased refractory period in ventricular muscle.
confirm elimination.
● Metabolism and Excretion: Treatment for Dysrhythmias:
○ 30% metabolized by the liver.
○ 50% to 70% excreted unchanged by ● Antidysrhythmics: Phenytoin and lidocaine (limited
kidneys. to short-term use).
○ Kidney dysfunction affects excretion;
thyroid dysfunction alters metabolism (dose
ANTIDOTE FOR CARDIAC/
adjustments may be needed for
DIGITALIS GLYCOSIDES
hypothyroidism and hyperthyroidism).
★ Digoxin Immune Fab (Digibind): Used to treat
Pharmacodynamics severe digitalis toxicity.
★ Mechanism: Binds with digoxin to form complex
● Effects: molecules that are excreted in urine, preventing
○ Increases myocardial contraction, digoxin from binding at cellular sites.
enhancing cardiac output and circulation. ★ Monitoring:
○ Decreases conduction through AV nodes, ○ Signs and symptoms of digoxin toxicity
resulting in a decreased heart rate. must be reported promptly to healthcare
● Therapeutic Serum Levels: providers.
○ 0.8 to 2.0 ng/mL. ○ Serum digoxin levels should be closely
○ Lower levels for heart failure; higher levels monitored.
for atrial fibrillation. ★ Potential Complications: Digitalis toxicity may lead
● Administration: Can be given orally or intravenously. to first-degree, second-degree, or complete heart
● Dosage and Considerations: Refer to Table 42-2 for block.
specific preparations and guidelines.
DRUG INTERACTIONS
DIGITALIS TOXICITY
Drug Interactions: Certain drugs can cause digitalis toxicity.
Digitalis Toxicity: Caused by overdose or accumulation of
digoxin.
Potent Diuretics: Furosemide (Lasix) and hydrochlorothiazide
(Esidrix, Microzide) lead to potassium loss (hypokalemia),
Signs and Symptoms: increasing digoxin's effect and risk of toxicity.

● Anorexia, diarrhea, nausea, vomiting.

Cortisone Preparations: Promote sodium retention and
● Bradycardia (pulse <60 beats/min).
potassium loss, also causing hypokalemia.
● Premature ventricular contractions, cardiac
dysrhythmias.

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Recommendations: NURSING PROCESS FOR CARDIAC

GLYCOSIDES: DIGOXIN
● Patients on digoxin with potassium-wasting diuretics
or cortisone should consume potassium-rich foods
or take supplements to prevent hypokalemia and
toxicity.

Antacids: Can decrease digoxin absorption if taken

simultaneously; doses should be staggered to avoid
interaction.

PHOSPHODIESTERASE INHIBITORS

Phosphodiesterase Inhibitors: A group of positive inotropic

drugs used to treat acute heart failure (HF).

Mechanism: Inhibit the enzyme phosphodiesterase,

promoting a positive inotropic response and vasodilation.

Example: Milrinone lactate increases stroke volume and

cardiac output while promoting vasodilation.

Administration: Given intravenously (IV) for no longer than

48 to 72 hours.

Monitoring: Close monitoring of the patient's

electrocardiogram (ECG) and cardiac status is essential due to
the risk of severe cardiac dysrhythmias.

OTHER AGENTS USED TO TREAT HEART FAILURE

Drug Groups for HF Treatment: Include vasodilators, ACE

Assessment
inhibitors, angiotensin II receptor antagonists (blockers),
diuretics (thiazides, furosemide), spironolactone (Aldactone),
● Drug and Herbal History: Check for interactions,
and some beta blockers.
especially with potassium-wasting diuretics or
cortisone.
Vasodilators: ● Pulse Rate: Obtain baseline apical pulse; it should be
>60 beats/min.
● Function: Decrease venous blood return to the ● Digitalis Toxicity Symptoms: Monitor for anorexia,
heart, reducing cardiac filling, ventricular stretching nausea, vomiting, bradycardia, dysrhythmias, and
(preload), and oxygen demand. visual disturbances; report immediately.
● Arteriolar Dilators' Effects:
1. Reduce cardiac afterload, increasing cardiac
output.
2. Dilate kidney arterioles, improving renal Nursing Diagnoses
perfusion and increasing fluid loss.
3. Enhance circulation to skeletal muscles. ● Decreased cardiac output related to impaired
pumping ability.

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● Ineffective peripheral tissue perfusion related to

HERBAL ALERT
cardiac output issues.
● Anxiety related to cardiac health threat.
• Ginseng may falsely elevate digoxin levels.
• St. John’s wort decreases absorption of digoxin and thus
Planning
decreases serum digoxin level.
• Psyllium (Metamucil) may decrease digoxin absorption.
● Patients will check their pulse daily before taking
• Hawthorn may increase the effect of digoxin.
digoxin.
• Licorice can potentiate the effect of digoxin. It promotes
● Patients will report pulse <60 beats/min or
potassium loss (hypokalemia), which increases the effect
significant decline.
of digoxin. It may cause digitalis toxicity.
● Patients will consume potassium-rich foods.
• Aloe may increase the risk of digitalis toxicity. It
increases potassium loss, which increases the effect of
Nursing Interventions
digoxin.
• Ma-huang or ephedra increases the risk of digitalis
● Check apical pulse before administration; withhold if
toxicity.
<60 beats/min.
• Goldenseal may decrease the effects of cardiac
● Monitor for peripheral/pulmonary edema signs.
glycosides and increase the effects of antidysrhythmics.
● Track serum digoxin (0.8-2 ng/mL) and potassium
levels (3.5-5.3 mEq/L); report hypokalemia.

Patient Teaching SUMMARY OF MEDICATIONS

FOR HEART FAILURE
● Emphasize adherence to therapy; involve a visiting
nurse if needed. ACE Inhibitors:
● Warn against OTC drug interactions without provider
consultation. ○ Dilate venules and arterioles, improving
● Keep medications away from children; request renal blood flow and reducing fluid volume.
childproof bottles. ○ Decrease aldosterone release, reducing
● Teach pulse checking before digoxin administration; sodium and fluid retention.
notify provider if <60 or irregular. ○ Monitor serum potassium levels, especially
● Report side effects: low pulse, nausea, vomiting, with potassium-sparing diuretics.
headache, diarrhea, visual disturbances. ● Angiotensin II Receptor Blockers (ARBs):
● Encourage a potassium-rich diet (fruits, vegetables). ○ Alternatives for patients intolerant to ACE
inhibitors (e.g., valsartan, candesartan).
Cultural Considerations ● Diuretics:
○ First-line treatment for fluid volume
● Address value conflicts and use culturally reduction, often used with digoxin.
appropriate communication. ○ Spironolactone: A potassium-sparing
● Ensure patients understand the importance of diuretic that blocks aldosterone, improving
medication adherence and potential side effects. heart rate variability and decreasing
● Consider cultural perspectives on authority and myocardial fibrosis. Monitor potassium
family involvement in healthcare decisions. levels closely.
● Beta Blockers:
Evaluation ○ Initially contraindicated but now beneficial
for HF when used cautiously (e.g.,
● Assess digoxin effectiveness through decreased carvedilol, metoprolol, bisoprolol).
heart rate and absence of side effects; continue ○ Start with low doses; effects may take 1 to
monitoring pulse rate. 3 months.

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● Nesiritide: ● Often indicates impending myocardial infarction

○ Atrial natriuretic peptide that promotes (MI); requires emergency intervention.
vasodilation and diuresis; useful for acute
decompensated HF with dyspnea. Variant (Prinzmetal, Vasospastic) Angina:
● BiDil:
○ Combination of hydralazine and isosorbide ● Occurs during rest due to vessel spasm (vasospasm).
dinitrate, approved for HF treatment,
particularly effective in African American Causes:
patients.
● Classic and unstable angina result from narrowing or
ANTIANGINAL DRUGS partial occlusion of coronary arteries.
● Variant angina is caused by coronary artery spasms.
I. Definition: Antianginal drugs treat angina pectoris,
characterized by acute cardiac pain from inadequate Co-occurrence: Patients may experience both classic and
blood flow to the myocardium. variant angina.
II. Causes:
A. Plaque occlusions in coronary arteries. NONPHARMACOLOGIC MEASURES
B. Spasms of the coronary arteries. TO CONTROL ANGINA
III. Effects: Decreased blood flow leads to reduced
oxygen supply to the myocardium, resulting in pain. ● Avoid:
IV. Symptoms: ○ Heavy meals
A. Described as tightness or pressure in the ○ Smoking
center of the chest. ○ Extreme weather changes
B. Pain may radiate down the left arm and can ○ Strenuous exercise
also be felt in the neck. ○ Emotional upset
V. Duration: Anginal pain typically lasts only a few ● Promote:
minutes. ○ Proper nutrition
VI. Risks: Anginal attacks can lead to myocardial ○ Moderate exercise (consult healthcare
infarction (heart attack). provider first)
VII. Diagnostic Tests: ○ Adequate rest
A. Stress tests. ○ Relaxation techniques
B. Echocardiogram.
C. Cardiac profile laboratory tests. These measures help prevent angina attacks.
D. Cardiac catheterization to assess blockage
in coronary arteries. TYPES OF ANGINAL DRUGS

Antianginal Drugs Overview

● Mechanism:
TYPES OF ANGINA PECTORIS ○ Increase blood flow by either:
■ Increasing oxygen supply
Classic (Stable) Angina: ■ Decreasing oxygen demand on the
myocardium
● Occurs with predictable stress or exertion. ● Types of Antianginals:
○ Nitrates:
Unstable (Preinfarction) Angina: ■ Major effect: Reduces venous
tone, decreases heart workload,
● Occurs frequently with increasing severity. promotes vasodilation
● Unpredictable regarding activity and intensity. ■ Effective for variant (vasospastic)
angina

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■ Administered sublingually and Other Forms:

intravenously for acute episodes
○ Beta Blockers: ● Topical (ointment, transdermal patch), translingual,
■ Decrease heart workload and oral extended-release capsules/tablets, aerosol
oxygen demands spray, IV.
■ Effective for stable angina
prevention Other Organic Nitrates:
■ Not effective for variant angina;
may worsen it ● Isosorbide Dinitrate: Available in SL, chewable,
○ Calcium Channel Blockers: immediate-release, and sustained-release forms.
■ Decrease heart workload and ● Isosorbide Mononitrate: Available in
oxygen demands immediate-release and sustained-release tablets.
■ Effective for variant angina ●
■ Substituted if beta blockers are
intolerable in acute care PHARMACOKINETICS AND PHARMACODYNAMICS
● Unstable Angina: OF NITROGLYCERIN
○ Requires immediate medical care
○ Treatment: Nitrates first; beta blockers or
calcium channel blockers as needed if pain
persists. ● Absorption:
○ Sublingual (SL) nitroglycerin is rapidly
NITRATES absorbed into the internal jugular vein and
right atrium.
Development: First agents for angina relief, developed in the ○ 40% to 50% of nitrates taken orally are
1840s. inactivated by first-pass metabolism in the
liver.
Mechanism: ○ Nitro-Bid ointment and Transderm-Nitro
patch absorb slowly through the skin.
● Cause generalized vascular and coronary ● Excretion: Primarily eliminated in urine.
vasodilation. ● Mechanism of Action:
● Increase blood flow to myocardial cells, reducing ○ Acts directly on smooth muscle of blood
myocardial ischemia. vessels, causing relaxation and dilation.
● Can cause hypotension. ○ Decreases cardiac preload (blood volume in
the ventricle at diastole) and afterload
Sublingual Nitroglycerin: (peripheral vascular resistance).
○ Reduces myocardial oxygen demand by
● Commonly used nitrate, average dose: 0.4 mg for decreasing blood return to the heart and
angina. peripheral resistance.
● Effects last approximately 10 minutes. ● Onset of Action:
● Must be kept in original airtight glass containers to ○ Rapid with SL and IV administration (1 to 3
prevent decomposition from heat and light. minutes).
● Not swallowed due to first-pass metabolism; ○ Slower with transdermal application (30 to
absorbed through sublingual vessels. 60 minutes).
● Duration of Action:
Administration Guidelines: ○ Transdermal patch: ~24 hours.
○ Nitro-Bid ointment: 6 to 8 hours (requires
● If pain persists after one dose, call 911. reapplication 3-4 times daily).
● Potential side effects include dizziness, faintness, or
headache due to vasodilation.

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● Tolerance Management:
○ Transdermal patches should be removed
nightly for an 8 to 12-hour nitrate-free ● Effectiveness:
interval to prevent tolerance. ○ Reduce myocardial oxygen consumption.
○ Effective for classic (stable) angina.
SIDE EFFECTS AND ADVERSE REACTIONS ● Administration Guidelines:
○ Do not abruptly discontinue; taper dose to
● Common Side Effects: avoid reflex tachycardia and angina
○ Headaches (may decrease with continued recurrence.
use; acetaminophen can help). ○ Contraindicated in patients with:
○ Hypotension. ■ Decreased heart rate and blood
○ Dizziness. pressure.
○ Weakness. ■ Second- or third-degree AV block.
○ Faintness. ● Types:
● Discontinuation: ○ Nonselective Beta Blockers:
○ Taper the dose over several weeks to ■ Block both beta1 and beta2 (e.g.,
prevent severe rebound pain due to propranolol, nadolol, pindolol).
myocardial ischemia. ■ Can cause bronchoconstriction.
● Reflex Tachycardia: ○ Selective (Cardiac) Beta Blockers:
○ Can occur if nitroglycerin is administered ■ Primarily block beta1 (e.g.,
too rapidly, leading to a significant increase atenolol, metoprolol).
in heart rate as the body compensates. ■ Preferred for angina control due to
lower risk of bronchoconstriction.
DRUG INTERACTION
NITROGLYCERIN AND ISOSORBIDE DINITRATE
Drug Interactions with Nitroglycerin
Short-Acting Nitroglycerin:
● Enhanced Hypotensive Effect:
○ Beta blockers. ● Forms: Nitrostat, Nitro-Bid, Transderm-Nitro.
○ Calcium channel blockers. ● Administration:
○ Vasodilators. ○ Sublingual (SL): 2.5-10 mg every 2-3 hours
○ Alcohol. as needed.
● Antagonistic Effect: ● Side Effects: Headaches, dizziness, lightheadedness,
○ IV nitroglycerin may antagonize the effects flushing.
of heparin. ● Pregnancy Category: C.
● Pharmacokinetics: Half-life 1-4 hours; tolerance
BETA BLOCKERS develops over time.

Beta-Adrenergic Blockers Overview Long-Acting Isosorbide Dinitrate:

● Function: ● Forms: Isordil, Sorbitrate.

○ Block beta1 and beta2 receptors. ● Administration:
○ Decrease sympathetic nervous system ○ PO (Immediate Release): Initially 5-20 mg
effects (block catecholamines). b.i.d./t.i.d.; maintenance 10-40 mg
○ Lower heart rate and blood pressure. b.i.d./t.i.d.
● Uses: ○ SR (Sustained Release): 40-160 mg/day to
○ Antianginal. prevent angina attacks.
○ Antidysrhythmic. ● Effects: Can lower blood pressure; tolerance may
○ Antihypertensive. develop.

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BETA BLOCKERS PHARMACOKINETICS AND Discontinuation:

PHARMACODYNAMICS
● Dosage should be tapered over 1-2 weeks to prevent
Pharmacokinetics: rebound effects, such as:
○ Reflex tachycardia
● Absorption: Well absorbed orally; sustained-release ○ Life-threatening cardiac dysrhythmias.
capsules have slow absorption.
● Half-lives: CALCIUM CHANNEL BLOCKERS
○ Propranolol (Inderal): 3-6 hours.
○ Atenolol (Tenormin): 6-7 hours. Introduction:
○ Metoprolol (Lopressor): 3-7 hours.
● Metabolism: Propranolol and metoprolol ● Introduced in 1982 for treating stable and variant
metabolized by the liver; atenolol absorbed 50% in angina, certain dysrhythmias, and hypertension.
GI, remainder excreted unchanged in feces.
● IV Administration: 85% of atenolol excreted in urine Mechanism of Action:
within 24 hours.
● Calcium activates myocardial contraction, increasing
Pharmacodynamics: heart workload and oxygen demand.
● CCBs:
● Decrease myocardial contraction force, reducing ○ Relax coronary artery spasms (for variant
oxygen demand. angina).
● Effective for classic (stable) angina. ○ Relax peripheral arterioles (for stable
● Onset and Duration: angina).
○ Propranolol: Onset 30 min, peak 1-1.5 ○ Decrease cardiac contractility (negative
hours, duration 4-12 hours. inotropic effect).
○ Atenolol: Onset 60 min, peak 2-4 hours, ○ Reduce afterload and peripheral resistance.
duration 24 hours. ○ Lower heart workload, thus reducing
○ Metoprolol: Onset 15 min, duration 6-12 oxygen demand.
hours.
Effects on Angina:
SIDE EFFECTS AND ADVERSE REACTIONS
● Variant (Vasospastic) Angina:
Effects: ○ Relaxation of coronary arteries.
● Classic (Stable) Angina:
● Both nonselective and selective beta blockers ○ Decrease in oxygen demand.
decrease heart rate and blood pressure.
Additional Resources:
Nonselective Beta Blockers:
● Treatment steps for classic and variant angina are
● Potential adverse reactions: detailed in Figure 42-1.
○ Bronchospasm ● Drug data, dosages, uses, and considerations for
○ Behavioral or psychotic responses CCBs are available in Table 42-4.
○ Impotence (e.g., with Inderal)
CALCIUM CHANNEL BLOCKERS
Monitoring: PHARMACOKINETICS AND PHARMACODYNAMICS

● Vital signs should be closely monitored in the early Key CCBs:

stages of therapy.
● Verapamil (Calan), Nifedipine (Procardia), Diltiazem
(Cardizem).

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Absorption: Drug Interactions:

● 80-90% absorbed via GI mucosa. ● Often combined with other antianginal drugs (e.g.,
● First-pass metabolism significantly reduces nitrates) to prevent angina.
bioavailability:
○ Verapamil: 20% Nifedipine Considerations:
○ Diltiazem: 45-65%
○ Nifedipine: 35-40%. ● Immediate-release forms (10- and 20-mg capsules)
linked to increased sudden cardiac death risk,
Protein Binding: especially at high doses.
● Sustained-release preparations (Procardia XL, Adalat
● Highly protein-bound (80-90% for the key CCBs; CC) do not carry the same risk.
>95% for others like Nicardipine, Amlodipine). ● Immediate-release Nifedipine typically used only in
hospital settings for acute blood pressure increases.
Half-Lives:
NURSING PROCESS
● Verapamil: 2-9 hours.
● Nicardipine: shortest at 5 hours. Assessment

Common Effects: ● Obtain baseline vital signs.

● Collect health and drug histories; note
● Bradycardia with Verapamil. contraindications (e.g., hypotension, acute
● Nifedipine promotes vasodilation, potentially myocardial infarction).
causing hypotension.
Nursing Diagnoses
Onset and Duration of Action:
● Decreased cardiac output related to poor myocardial
● Verapamil: Onset 10 minutes, duration 3-7 hours perfusion.
(oral), 2 hours (IV). ● Anxiety related to perceived threat of death.
● Nifedipine and Diltiazem: Onset 30 minutes, ● Acute pain related to anginal pain from inadequate
duration 6-8 hours. coronary perfusion.
● Activity intolerance related to lack of oxygen due to
SIDE EFFECTS AND ADVERSE REACTIONS poor perfusion.

Common Side Effects: Planning

● Headache. ● Control patient’s angina pain with nitroglycerin or
● Hypotension (more common with Nifedipine). other antianginals.
● Dizziness.
● Flushing of the skin.
Nursing Interventions

● Monitor vital signs; watch for hypotension.

● Position patient sitting or lying down during initial
Additional Effects:
nitrate use; check vital signs in different positions.
● Offer water before administering sublingual nitrates
● Reflex tachycardia (due to hypotension).
to aid absorption.
● Peripheral edema (notably with Nicardipine,
● Monitor IV nitroglycerin effects; report persistent
Nifedipine, Verapamil).
angina.
● Possible changes in liver and kidney function;
● Apply Nitro-Bid ointment with non-absorbent tools;
periodic monitoring of serum liver enzymes is
avoid areas near defibrillator paddles.
recommended.

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Patient Teaching ● Terminology: Dysrhythmia (disturbed rhythm) and

arrhythmia (absence of rhythm) are often used
General: interchangeably.

● Use SL nitroglycerin for chest pain; call 911 if there is ECG Analysis
no relief in 5 minutes.
● Avoid alcohol to prevent hypotension. ● P Wave: Atrial activation.
● Report if chest pain is not fully alleviated; tolerance ● QRS Complex: Ventricular depolarization.
may develop. ● T Wave: Ventricular repolarization.
● Do not discontinue beta or calcium blockers without ● P-R Interval: AV conduction time.
approval. ● Q-T Interval: Ventricular action potential duration.

Self-Administration: Impact on Cardiac Output

● Demonstrate SL nitroglycerin use (under tongue). ● Atrial Dysrhythmias: Decrease cardiac output by
● Store medication away from light in original amber 33% due to poor ventricular filling.
glass. ● Ventricular Dysrhythmias: Life-threatening; can lead
● Apply Transderm-Nitro patch once daily; rotate to ineffective pumping and decreased or absent
application sites. cardiac output.
● Seek medical attention if pain persists.
Risks and Causes
Side Effects
● Ventricular Tachycardia: Can progress to ventricular
● Suggest acetaminophen for headache relief. fibrillation and death; CPR is essential.
● Position supine with elevated legs if hypotension ● Common Causes: Follow myocardial infarction,
occurs. hypoxia, hypercapnia, thyroid disease, coronary
● Instruct on pulse rate monitoring. artery disease, cardiac surgery, excess
● Notify the provider if dizziness or faintness occurs catecholamines, electrolyte imbalances.
with beta or calcium blockers.
PHARMACODYNAMICS OF
Cultural Considerations ANTIDYSRHYTHMIC DRUGS
● Address dietary influences on cardiac health. Block Adrenergic Stimulation: Reduces heart rate and
● Use printed materials in the patient's preferred contractility by inhibiting sympathetic nervous system
language; consider an interpreter for effective activity.
communication.
Depress Myocardial Excitability and Contractility: Decreases
Evaluation the heart's responsiveness and force of contraction.

● Assess response to nitrates for angina pain relief; Decrease Conduction Velocity: Slows down electrical
monitor for headache, dizziness, or faintness. impulses in cardiac tissue, reducing heart rate.

ANTIDYSRHYTHMIC DRUGS Increase Recovery Time (Repolarization): Prolongs the time

it takes for the myocardium to reset after contraction.
Cardiac Dysrhythmias Overview
Suppress Automaticity: Reduces spontaneous depolarization,
● Definition: Any deviation from normal heartbeat preventing unintended heartbeats.
rate or pattern (bradycardia, tachycardia, irregular
rhythms).

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CARDIAC ACTION POTENTIAL CLASS I: CALCIUM CHANNEL BLOCKERS

● Electrolyte Transfer: Sodium and calcium enter ● Mechanism: Decreases sodium influx into cardiac
cardiac cells, leading to depolarization (contraction). cells.
○ Sodium: Rapid influx initiates ● Responses:
depolarization. ○ Decreased conduction velocity in cardiac
○ Calcium: Enters later to maintain tissues.
depolarization; triggers release of more ○ Suppressed automaticity, reducing ectopic
calcium from the sarcoplasmic reticulum. foci likelihood.
○ Increased recovery time (prolonged
Phases of Cardiac Action Potential refractory period).

1. Phase 0: Rapid depolarization due to sodium influx. Subgroups of Sodium Channel Blockers:
2. Phase 1: Initial repolarization; termination of sodium
influx. 1. Class IA:
3. Phase 2: Plateau phase; calcium influx prolongs ○ Drugs: Quinidine, Procainamide,
action potential and promotes contraction. Disopyramide.
4. Phase 3: Rapid repolarization due to potassium ○ Effect: Slows conduction, prolongs
influx. repolarization.
5. Phase 4: Resting membrane potential; flat in 2. Class IB:
ventricular muscle but rises in SA node cells as they ○ Drugs: Lidocaine, Mexiletine HCl.
prepare for the next heartbeat. ○ Effect: Slows conduction, shortens
repolarization.
Additional Notes ○ Lidocaine:
■ Initially a local anesthetic;
● Myocardial ischemia can lead to irregular discovered to have
contractions. antidysrhythmic properties.
■ Used for acute ventricular
TYPES OF DYSRHYTHMIC DRUGS dysrhythmias.
■ Rapid onset of action (IV).
Desired Action: Restore normal cardiac rhythm. ■ Approximately one-third reaches
general circulation.
Drug Classes: 3. Class IC:
○ Drug: Flecainide.
1. Sodium (fast) Channel Blockers: IA, IB, IC. ○ Effect: Prolongs conduction with little to no
2. Beta Blockers: Reduce adrenergic stimulation. effect on repolarization.
3. Drugs that Prolong Repolarization: Extend recovery
time of myocardial cells. CLASS II: BETA BLOCKERS
4. Calcium (slow) Channel Blockers: Decrease
conduction velocity and myocardial contractility. ● Mechanism: Decrease conduction velocity,
automaticity, and recovery time (refractory period).
Tables: ● Examples: Propranolol (Inderal), Acebutolol
(Sectral), Esmolol (Brevibloc), Sotalol (Betapace).
● Table 42-5: Lists classes, actions, and indications. ● Usage: More frequently prescribed for dysrhythmias
● Table 42-6: Lists commonly administered than sodium channel blockers.
antidysrhythmics with dosages, uses, and
considerations. Acebutolol (Sectral) Details

● Pharmacokinetics:
○ Well absorbed in the GI tract.

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○ Metabolized in the liver to active

metabolites.
○ 50%-60% eliminated in bile (feces), ● Lidocaine:
30%-40% excreted in urine. ○ High doses: Cardiovascular depression,
○ Half-life: 3-4 hours; metabolites: 8-13 bradycardia, hypotension, seizures, blurred
hours. vision, double vision.
● Pharmacodynamics: ○ Less serious: Dizziness, lightheadedness,
○ Indications: Ventricular dysrhythmias, confusion.
angina pectoris, hypertension. ○ Contraindicated: Advanced AV block;
○ Onset of action: 1 hour. caution in liver disorder and heart failure
○ Peak time: 4-6 hours. (HF).
○ Duration of action: 10 hours for ● Mexiletine and Tocainide:
dysrhythmias; 20-24 hours for ○ Similar side effects to lidocaine;
hypertension. contraindicated in cardiogenic shock and
second-/third-degree heart block.
CLASS III: DRUGS THAT PROLONG REPOLARIZATION ● Beta Blockers:
○ Side effects: Bradycardia, hypotension.
Mechanism: Prolong repolarization and increase the ● Bretylium and Amiodarone:
refractory period. ○ Side effects: Nausea, vomiting,
hypotension, neurologic problems.
Primary Use: Emergency treatment of ventricular ● Calcium Channel Blockers:
dysrhythmias when other antidysrhythmics are ineffective. ○ Side effects: Nausea, vomiting,
hypotension, bradycardia.
Example: Amiodarone (Cordarone).
Additional Considerations
● Effects: Increases refractory period and prolongs
action potential duration (cardiac cell activity). ● All antidysrhythmic drugs are potentially
prodysrhythmic; can induce life-threatening
CLASS IV: CALCIUM CHANNEL BLOCKERS ventricular dysrhythmias.
● Therapy is often initiated with continuous cardiac
● Drugs: Calcium channel blockers (e.g., Verapamil, monitoring in hospital settings.
Diltiazem).
● Mechanism: Block calcium influx, decreasing DIURETICS
myocardial excitability and contractility (negative
inotropic effect). ● Purpose: Decrease hypertension and reduce edema
● Effects: Increase refractory period of the AV node, (peripheral and pulmonary) in heart failure (HF) and
reducing ventricular response. renal/liver disorders.
● Contraindications: Not suitable for patients with AV ● Mechanism: Increase urine flow (diuresis) by
block or heart failure (HF). inhibiting sodium and water reabsorption in kidney
tubules.
SIDE EFFECTS AND ADVERSE REACTIONS OF
ANTIDYSRHYTHMIC DRUGS Renal Function

● Quinidine: ● Filtration: Every 1.5 hours, extracellular fluid (ECF) is

○ Side effects: Nausea, vomiting, diarrhea, filtered through kidneys; small particles
confusion, hypotension, heart block, (electrolytes, drugs, glucose, waste) are filtered;
neurologic and psychiatric symptoms. larger products (proteins, blood cells) remain in
● Procainamide: circulation.
○ Less cardiac depression than quinidine. ● Sodium Reabsorption:
○ 99% of filtered sodium is reabsorbed.

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○ Locations: 50-55% in proximal tubules, THIAZIDE AND THIAZIDE-LIKE DIURETICS

35-40% in loop of Henle, 5-10% in distal
tubules, <3% in collecting tubules. ● Introduction: Chlorothiazide (Diuril) was the first
thiazide, marketed in 1957, followed by
Diuretic Categories hydrochlorothiazide.
● Action: Act on the distal convoluted renal tubule to
1. Thiazide and thiazide-like promote sodium, chloride, and water excretion.
2. Loop (high-ceiling) ● Uses: Primarily for treating hypertension and
3. Osmotic peripheral edema; not effective for immediate
4. Carbonic anhydrase inhibitor diuresis.
5. Potassium-sparing ● Renal Considerations:
○ Ineffective if creatinine clearance is <30
Effects and Considerations mL/min.
○ Not recommended for patients with severe
● Antihypertensive Effect: Promote sodium and water renal dysfunction.
loss, lowering fluid volume and blood pressure.
● Electrolyte Loss: Many diuretics cause loss of Effects and Side Effects
potassium, magnesium, chloride, and bicarbonate.
○ Potassium-Wasting Diuretics: Promote ● Electrolyte Loss: Causes loss of sodium, potassium,
potassium excretion. and magnesium.
● Calcium Reabsorption: Promotes calcium
reabsorption, potentially leading to hypercalcemia,
which can be hazardous for patients on digitalis or
those with cancer.
● Glucose Tolerance: May affect glucose tolerance,
leading to hyperglycemia; use cautiously in patients
with diabetes.
● Monitoring: Laboratory tests (electrolytes, glucose)
should be regularly monitored.

Combination Therapy

● Hydrochlorothiazide is often combined with ACE

inhibitors, beta-blockers, alpha-blockers, angiotensin
II blockers, and centrally acting sympatholytics to
manage hypertension.

PHARMACOKINETICS AND PHARMACODYNAMICS

Pharmacokinetics and Pharmacodynamics of Thiazides

○ Potassium-Sparing Diuretics: Retain ● Absorption: Thiazides are well absorbed from the
potassium. gastrointestinal (GI) tract.
● Protein Binding: Hydrochlorothiazide has moderate
Combination Diuretics protein-binding capacity.
● Half-Life: Thiazides have a longer half-life compared
● Often marketed for hypertension, combining to loop diuretics; administered in the morning to
potassium-wasting and potassium-sparing diuretics prevent nocturia.
for additive blood pressure reduction effects.

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Pharmacodynamics CONTRAINDICATIONS

● Vasodilation: Thiazides act directly on arterioles to ● Renal Failure: Thiazides are contraindicated in
cause vasodilation, lowering blood pressure. patients with renal failure.
● Fluid Excretion: Promote sodium chloride and water ● Symptoms of Severe Kidney Impairment:
excretion, decreasing vascular fluid volume, cardiac ○ Oliguria (marked decrease in urine output)
output, and blood pressure. ○ Elevated blood urea nitrogen (BUN)
● Onset of Action: Hydrochlorothiazide onset occurs ○ Elevated serum creatinine
within 2 hours; peak concentration is 3 to 6 hours.
DRUG INTERACTIONS
Duration of Action
Thiazide Drug Interactions
● Classification: Thiazides are divided into three
groups based on duration: ● Digoxin:
○ Short-acting: Less than 12 hours ○ Thiazides can cause hypokalemia,
○ Intermediate-acting: 12 to 24 hours increasing the risk of digoxin toxicity.
○ Long-acting: More than 24 hours ○ Thiazides induced hypercalcemia, further
enhancing digoxin's effects.
SIDE EFFECTS AND ADVERSE REACTIONS ○ Monitor for signs of digitalis toxicity:
bradycardia, nausea, vomiting, visual
changes.
Side Effects and Adverse Reactions of Thiazides ● Lithium:
○ Thiazides enhance lithium's action,
● Electrolyte Imbalances: increasing the risk of lithium toxicity.
○ Hypokalemia (low potassium) ● Antihypertensive Drugs:
○ Hypercalcemia (high calcium) ○ Thiazides potentiate the effects of other
○ Hypomagnesemia (low magnesium) antihypertensives, useful for combination
○ Bicarbonate loss therapy in hypertension.
● Metabolic Effects:
○ Hyperglycemia (elevated blood sugar)
○ Hyperuricemia (elevated serum uric acid) LOOPS (HIGH CEILING) DIURETICS
○ Hyperlipidemia (elevated blood lipid levels)
● Monitoring: Mechanism of Action:
○ Regular assessment of serum potassium,
calcium, and uric acid levels. ● Act on the thick ascending loop of Henle.
○ Potassium supplements may be needed. ● Inhibit chloride transport of sodium, leading to
● Other Side Effects: sodium and water loss, along with potassium,
○ Dizziness calcium, and magnesium.
○ Headache
○ Nausea Potency:
○ Vomiting
○ Constipation ● Extremely potent, causing significant depletion of
○ Rarely: Urticaria (hives) and blood water and electrolytes.
dyscrasias. ● More effective than thiazides for diuresis (2-3 times
● Considerations: A drug may be needed to lower more effective) but less effective as antihypertensive
blood lipid levels due to thiazide-induced increases. agents.

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Administration: ● Daily weight monitoring; a 2.2 lb gain equals 1 L of

fluid.
● Typically given as an oral dose in the morning; IV for ● Note urine output for fluid loss/retention.
immediate fluid removal in acute conditions (e.g.,
heart failure, pulmonary edema). Patient Teaching

General:
Combination Use:
● Stress adherence to medication; effects may take
● Avoid using another loop diuretic. time.
● Can combine with thiazide if furosemide alone is ● Suggest morning dosing to avoid nocturia.
ineffective. ● Keep medications out of children's reach; use
childproof bottles.
Effects on Electrolytes: ● Warn about herbal interactions.

● May affect blood sugar and increase uric acid levels. Self-Administration:

NURSING PROCESS ● Teach blood pressure monitoring and recording.

Assessment Side Effects:

● Monitor vital signs, weight, urine output, and serum ● Advise gradual position changes to prevent
chemistry (electrolytes, glucose, uric acid). dizziness.
● Check for peripheral edema, noting any pitting. ● Monitor blood sugar for prediabetics.
● Review patient's drug and herbal supplement history ● Use sunblock due to photosensitivity.
for potential interactions (e.g., digoxin,
corticosteroids, antidiabetics). Diet:

Nursing Diagnoses ● Encourage potassium-rich foods; potassium

supplements may be necessary.
● Risk for deficient fluid volume related to thiazide ● Recommend taking medication with food to prevent
use. GI upset.
● Impaired urinary elimination related to kidney
dysfunction. Cultural Considerations
● Excess fluid volume related to retention.
● Respect cultural practices; ensure adequate
Planning potassium intake or supplements if dietary
restrictions exist.
● Goal: Decrease blood pressure to normal. ● Highlight the importance of potassium
● Goal: Reduce edema. supplementation with potassium-wasting diuretics.
● Goal: Maintain serum chemistry within normal
ranges. Evaluation

Nursing Interventions ● Assess effectiveness of therapy: reduced blood

pressure and edema, normal blood chemistry.
● Monitor vital signs and electrolytes, especially ● Ensure absence of side effects and adverse
potassium and glucose. reactions.
● Observe hypokalemia symptoms (muscle weakness,
leg cramps, dysrhythmias).

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● Duration of Action: Shorter than that of thiazides.

HERBAL ALERT SIDE EFFECTS AND ADVERSE REACTIONS

● Aloe: Can decrease serum potassium levels, causing ● Common Side Effects:
hypokalemia when combined with ○ Fluid and electrolyte imbalances (e.g.,
potassium-wasting diuretics (e.g., thiazides). hypokalemia, hyponatremia, hypocalcemia,
● Gingko: May increase blood pressure when taken hypomagnesemia, hypochloremia).
with thiazide diuretics. ○ Hypochloremic metabolic alkalosis may
● Licorice: Can increase potassium loss, leading to worsen hypokalemia.
hypokalemia. ○ Orthostatic hypotension.
● Hawthorne: May potentiate hypotension. ● Rare Effects:
○ Thrombocytopenia.
CONTRAINDICATIONS ○ Skin disturbances.
○ Transient deafness.
★ Renal Blood Flow: Loop diuretics can increase renal ● Note: Table 43-3 details physiological and laboratory
blood flow by up to 40%. changes associated with loop diuretics.
★ Furosemide Use: Frequently prescribed for patients
with creatinine clearance <30 mL/min and end-stage DRUG INTERACTIONS
renal disease.
★ Calcium Excretion: Loop diuretics cause excretion of Major Drug Interaction:
calcium, unlike thiazides, which inhibit calcium loss.
★ Loop Diuretics: Ethacrynic acid (Edecrin) was the ● Loop diuretics can interact with digitalis
first marketed, followed by furosemide (Lasix) and preparations (digoxin).
bumetanide (Bumex), which is more potent on a
mg-for-mg basis. Risk of Toxicity:
★ Sulfonamide Derivatives: Furosemide and
bumetanide are sulfonamide derivatives; ethacrynic ● Hypokalemia from loop diuretics enhances the
acid is reserved for patients allergic to sulfa drugs. effects of digoxin, increasing the risk of digitalis
toxicity.
PHARMACOKINETICS AND PHARMACODYNAMICS
Potassium Management:
Pharmacokinetics
● Patients may need potassium replacement through
● Absorption: Rapidly absorbed from the GI tract. food or supplements.
● Protein Binding: Highly protein-bound; competes for ● Close monitoring of serum potassium levels is
binding sites with other drugs. essential, especially at high doses of loop diuretics.
● Half-Life: Varies from 30 minutes to 1.5 hours.
OSMOTIC DIURETICS
PharmacodynamicsSaluretic Effect: Significant
sodium-chloride (saluretic) and sodium (natriuretic) effect; Osmotic Diuretics:
rapid diuresis reduces vascular fluid volume, cardiac output,
and blood pressure. ● Increase osmolality and sodium reabsorption in the
proximal tubule and loop of Henle.
● Potency: Furosemide is more potent than thiazides, ● Excrete sodium, chloride, potassium (to a lesser
increasing renal blood flow before diuresis. degree), and water.
● Dosing: Oral dose of furosemide is typically twice
the IV dose. Uses:
● Onset of Action: 30 to 60 minutes for oral; 5
minutes for IV. ● Prevent kidney failure.

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● Decrease intracranial pressure (ICP) (e.g., in cerebral Effects: Increase excretion of sodium, potassium, and
edema). bicarbonate; prolonged use can lead to metabolic acidosis.
● Decrease intraocular pressure (IOP) (e.g., in
glaucoma). Primary Use: Decrease intraocular pressure (IOP) in
open-angle (chronic) glaucoma; not for narrow-angle or acute
Mannitol: glaucoma.

● Potent osmotic potassium-wasting diuretic, Other Uses: Diuresis, management of epilepsy, treatment of
commonly used in emergencies (ICP and IOP). high-altitude or acute mountain sickness.
● Can be combined with cisplatin and carboplatin in
cancer chemotherapy to induce diuresis and reduce Combination: May be alternated with loop diuretics; useful in
side effects. metabolic alkalosis needing diuretic.
● Diuresis occurs within 1 to 3 hours after IV
administration. SIDE EFFECTS AND DIVERSE REACTIONS

Other Diuretics: Side Effects of Acetazolamide:

● Urea is also used but less frequently than mannitol. ● Fluid and Electrolyte Imbalance
● Metabolic Acidosis
SIDE EFFECTS AND ADVERSE REACTIONS ● Nausea and Vomiting
● Anorexia
● Confusion
● Side Effects and Adverse Reactions of Mannitol: ● Orthostatic Hypotension
○ Fluid and electrolyte imbalance. ● Crystalluria
○ Pulmonary edema from rapid fluid shifts. ● Hemolytic Anemia
○ Nausea and vomiting. ● Renal Calculi
○ Tachycardia due to rapid fluid loss.
○ Acidosis. Contraindication: Not recommended during the first
● Crystallization: trimester of pregnancy.
○ Crystallization can occur when exposed to
low temperatures. POTASSIUM-SPARING DIURETICS
○ Vial should be warmed to dissolve crystals.
○ Do not use mannitol solution for IV infusion
if crystals are present and undissolved ● Potassium-Sparing Diuretics:
○ Weaker than thiazides and loop diuretics;
CONTRAINDICATIONS used as mild diuretics or in combination.
○ Continuous use of potassium-wasting
● Cautions for Mannitol Use: diuretics requires potassium supplements;
○ Administer with extreme caution in patients not needed with potassium-sparing
with heart disease and heart failure (HF). diuretics.
○ Immediately discontinue if the patient ○ Hyperkalemia Risk: Serum potassium
develops heart failure or renal failure. should be monitored; discontinue if >5.3
mEq/L and restrict high-potassium foods.
CARBONIC ANHYDRASE INHIBITORS ● Mechanism of Action:
○ Act in collecting duct and late distal tubule.
Examples: Acetazolamide, dichlorphenamide, ethoxzolamide, ○ Promote sodium and water excretion while
methazolamide. retaining potassium.
○ Interfere with sodium-potassium pump
Mechanism: Block carbonic anhydrase, affecting acid-base controlled by aldosterone.
balance (hydrogen and bicarbonate ions). ● Key Potassium-Sparing Diuretics:

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○ Spironolactone (Aldactone): First

potassium-sparing diuretic; blocks Essential Hypertension: Most common type, affecting 90% of
aldosterone, promotes potassium individuals with high blood pressure; origin unknown.
retention. Effects take 48 hours.
○ Amiloride (Midamor) and Triamterene Contributing Factors: Family history, hyperlipidemia,
(Dyrenium): Used for edema in heart African-American background, diabetes, aging, stress,
failure or liver cirrhosis. excessive alcohol, smoking, and obesity.
○ Eplerenone (Inspra): Effective
antihypertensive agent. Secondary Hypertension: Accounts for 10% of cases; linked
● Combination Use: to renal and endocrine disorders.
○ Often combined with potassium-wasting
diuretics (e.g., hydrochlorothiazide) to SELECTED REGULATORS OF BLOOD PRESSURE
enhance diuretic effect and prevent
potassium loss. Kidney and Blood Pressure Regulation:
○ Common combinations include:
■ Spironolactone + ● Kidneys control fluid volume and the
Hydrochlorothiazide (Aldactazide) renin-angiotensin-aldosterone system (RAAS).
■ Amiloride + Hydrochlorothiazide ● Sodium and water elimination/retention affects
(HCTZ) cardiac output and systemic arterial blood pressure.
■ Triamterene +
Hydrochlorothiazide (Dyazide, Renin-Angiotensin-Aldosterone System (RAAS):
Maxzide)
● Caution: Avoid use with ACE inhibitors and ARBs due ● Renin is released from renal cells.
to potential for increased serum potassium. ● Renin stimulates production of angiotensin II (potent
vasoconstrictor).
SIDE EFFECTS AND DIVERSE REACTIONS ● Angiotensin II prompts release of aldosterone
(promotes sodium and water retention).
● Increased sodium and water retention raises fluid
● Main Side Effect: Hyperkalemia is the primary volume and blood pressure.
concern with potassium-sparing diuretics.
● Renal Function Caution: Use cautiously in patients
Additional Regulators:
with poor renal function; kidneys excrete 80-90% of
potassium.
● Baroreceptors: Located in the aorta and carotid
● Urine Output Requirement: Ensure urine output is
sinus; detect changes in blood pressure.
at least 600 mL/day.
● Vasomotor Center: Located in the medulla; helps
● Potassium Supplementation: Avoid potassium
regulate blood pressure.
supplements unless serum potassium is low.
● Catecholamines:
● Drug Interaction Risk: Combining potassium-sparing
○ Norepinephrine (from sympathetic nerves)
diuretics with ACE inhibitors can lead to severe or
and epinephrine (from adrenal medulla)
life-threatening hyperkalemia.
increase blood pressure via
● Monitoring: Regular monitoring of serum potassium
vasoconstriction.
levels is essential for safe therapy.
● Gastrointestinal Disturbances: Possible side effects
include anorexia, nausea, vomiting, diarrhea, and Other Hormones:
numbness/tingling in extremities.
● Antidiuretic Hormone (ADH):
○ Produced by hypothalamus, stored and
ANTIHYPERTENSIVES released by posterior pituitary.
○ Conserves water during fluid volume
Definition of Hypertension: Systolic pressure >140 mm Hg
deficit; inhibited during fluid overload.
and diastolic pressure >90 mm Hg.

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● Atrial Natriuretic Peptide (ANP) and Brain

Natriuretic Peptide (BNP): Contribute to blood
pressure regulation. ● Hypertension in Asian Americans:
○ Twice as sensitive to beta blockers and
PSYCHOLOGICAL RISK FACTOR other antihypertensives compared to
whites.
○ Often requires reduced dosing.
● Physiologic Risk Factors for Hypertension: ● Hypertension in Native Americans:
○ Diet: ○ Lower response to beta blockers compared
■ High in saturated fats and simple to whites.
carbohydrates increases blood ● Monitoring:
pressure. ○ Ongoing assessment of blood pressure and
■ Carbohydrate intake affects drug dosing is essential for these cultural
sympathetic nervous activity. groups.
○ Alcohol:
■ Increases renin secretion, leading HYPERTENSION IN OLDER ADULTS
to higher angiotensin II
production. ● Hypertension Prevalence in Older Adults:
○ Obesity: ○ By age 65: 26% of men and 30% of women
■ Increases cardiac output, stroke are hypertensive.
volume, and left ventricular filling. ○ Ages 65-75: 30% of men and 45% of
■ Two-thirds of hypertensive women are hypertensive.
individuals are obese. ● Cardiovascular Risks:
○ Weight Loss: ○ Both systolic and diastolic hypertension are
■ Can decrease hypertension. linked to increased morbidity and mortality.
■ Mild to moderate sodium ○ Antihypertensive therapy can reduce
restriction also helps reduce blood cardiovascular disorders:
pressure. ■ 34% decrease in stroke risk.
■ 19% decrease in coronary heart
CULTURAL RESPONSES TO HYPERTENSIVE AGENTS disease risk.
● Side Effects of Antihypertensive Agents:
○ Orthostatic Hypotension:
● Hypertension in African Americans: ■ Common in older adults,
○ Develop hypertension at an earlier age than particularly frail or institutionalized
white Americans. individuals.
○ Higher mortality rate from hypertension ■ Causes dizziness due to sudden
compared to whites. low blood pressure when standing
○ Beta blockers and ACE inhibitors are less up.
effective unless combined with diuretics. ■ The sympathetic nervous system
○ Susceptible to low-renin hypertension; do response is slower in older adults,
not respond well to beta blockers and ACE worsened by antihypertensive
inhibitors. medications.
○ Effective antihypertensive drugs: alpha1 ■ May require dosage adjustments
blockers and calcium channel blockers. or alternative medications if
○ Diuretics can be effective as initial orthostatic hypotension occurs.
monotherapy. ● Lifestyle Modifications for Older Adults with
● Hypertension in White Patients: Hypertension:
○ Typically have high-renin hypertension. ○ Restrict dietary sodium to 2400 mg daily.
○ Respond well to all antihypertensive agents. ○ Avoid tobacco.
○ Modify diet and exercise.

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○ Decrease stress. PHARMACOLOGIC CONTROL FOR HYPERTENSION

NON PHARMACOLOGICAL CONTROL Individualized Approach to Hypertension Treatment:

OF HYPERTENSION
● Focus on initial agents for hypertension
Nonpharmacologic Methods to Decrease Blood Pressure: management.
● Emphasize reduction of other cardiovascular risk
● Effective for reducing blood pressure. factors.
● Recommended when systolic pressure is ≤140 mm ● Aim for fewer drugs at the lowest effective doses,
Hg. substituting instead of adding.
● Methods include:
○ Stress-reduction techniques. Use of Antihypertensives:
○ Exercise.
○ Salt restriction. ● Often, multiple antihypertensives are used for better
○ Decreased alcohol intake. control and fewer side effects.
○ Smoking cessation.
Classification of Antihypertensive Drugs:
Use of Antihypertensive Drugs:
1. Diuretics.
● Prescribed when hypertension is uncontrolled by 2. Sympatholytics (sympathetic depressants).
nonpharmacologic means. 3. Direct-acting arteriolar vasodilators.
● Nonpharmacologic methods should be combined 4. ACE inhibitors.
with antihypertensive drugs for optimal 5. Angiotensin II receptor blockers (ARBs).
hypertension management. 6. Calcium channel blockers.

GUIDELINES FOR HYPERTENSION DIURETICS

Diuretics Overview:
Blood Pressure Guidelines (JNC 7):
● Promote sodium depletion, decreasing extracellular
● Normal: <120/80 mm Hg. fluid volume (ECFV).
● Prehypertension: SBP 120-139 mm Hg; DBP 80-89 ● Effective as first-line treatment for mild
mm Hg. hypertension.
● Stage 1 Hypertension: 140-159/90-99 mm Hg.
● Stage 2 Hypertension: ≥160/100 mm Hg. Hydrochlorothiazide (HCTZ):

● Most frequently prescribed diuretic for mild

hypertension.
Hypertension Treatment: ● Can be used alone or in combination with other
antihypertensives.
● Two-thirds of hypertensive patients have
uncontrolled or suboptimal treatment. Combination Therapy:
● SBP is a more significant CVD risk factor for those
aged 50 and older. ● Diuretics are often used with other antihypertensive
● If blood pressure is >20/10 mm Hg above goal, agents to prevent fluid retention.
initiate drug therapy. ● Thiazide diuretics are not recommended for patients
● CVD risk doubles with each increase of 20/10 mm with renal insufficiency (creatinine clearance <30
Hg, starting from 115/75 mm Hg. mL/min).
● Loop diuretics (e.g., furosemide) are preferred in
such cases as they do not depress renal blood flow.

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Considerations for Diuretics: ● Types of Beta Blockers:

○ Nonselective: Propranolol, carvedilol (block
● Loop diuretics may elevate serum renin levels; avoid both beta1 and beta2).
hypertension is due to the ○ Cardioselective: Acebutolol, atenolol,
renin-angiotensin-aldosterone system. betaxolol, bisoprolol, metoprolol (mainly
● Combining potassium-wasting and block beta1, less bronchoconstriction).
potassium-sparing diuretics may reduce potassium ● Bronchoconstriction Risks:
loss. ○ Cardioselectivity does not guarantee
protection; caution in patients with
Thiazide Combinations: bronchospasm or pulmonary disease.
● Combination Therapy:
● Thiazides can be combined with other ○ Often combined with hydrochlorothiazide
antihypertensives to enhance effectiveness. (12.5-25 mg dose).
● Common combinations include thiazides with ● Contraindications:
potassium-sparing diuretics, beta blockers, ACE ○ Not for patients with second- or
inhibitors, or angiotensin II receptor blockers. third-degree AV block or sinus bradycardia.
● ACE inhibitors increase serum potassium levels, ○ Non Cardioselective beta blockers should
minimizing potassium loss when combined with not be used in COPD patients.
thiazide diuretics. ● Pharmacokinetics:
○ Metoprolol is well absorbed; short half-life
and low protein binding.
Sympatholytics (Sympathetic Depressants) ● Pharmacodynamics:
○ Cardioselective blockers lower heart rate
Sympatholytics Overview: and blood pressure; non selective blockers
can cause bronchoconstriction.
● Comprise five drug groups: ○ Cross the placental barrier and excreted
1. Beta-adrenergic blockers: Block beta breast milk.
receptors. ● Onset and Duration:
2. Centrally acting alpha2 agonists. ○ Oral onset: ~30 minutes; duration: 6-12
3. Alpha-adrenergic blockers: Block alpha hours.
receptors. ○ IV onset: immediate; peak at 20 minutes.
4. Adrenergic neuron blockers: Peripherally
acting sympatholytics.
5. Alpha1- and beta1-adrenergic blockers. SIDE EFFECTS AND ADVERSE REACTIONS

● Common Side Effects:

Beta-Adrenergic Blockers ○ Decreased pulse rate
○ Markedly decreased blood pressure
Beta-adrenergic Blockers Overview: ○ Bronchospasm (with non cardioselective
beta blockers)
○ Used as antihypertensives, antianginals, ○ Dizziness
and antidysrhythmics. ○ Insomnia
○ Reduce cardiac output by decreasing ○ Depression
sympathetic nervous system response. ○ Fatigue
○ Lower heart rate, contractility, and renin ○ Nightmares
release; more effective in patients with ○ Sexual dysfunction
higher renin levels. ● Serious Risks of Abrupt Discontinuation:
● Response in African Americans: ○ Rebound hypertension
○ Less effective alone for hypertension; ○ Angina
better combined with diuretics. ○ Dysrhythmias

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○ Myocardial infarction
● Special Considerations:
○ Use with caution in diabetes mellitus due ● Additional Information:
to: ○ Table 44-1 includes centrally acting alpha2
■ Inhibition of glycogen conversion agonists along with beta blockers.
to glucose during hypoglycemia
■ Masking of tachycardia symptoms SIDE EFFECTS AND ADVERSE REACTIONS
associated with hypotension
● Additional Information: ● Common Side Effects:
○ Further side effects discussed in Chapter ○ Drowsiness
42. ○ Dry mouth
○ Table 44-1 provides a list of beta blockers ○ Dizziness
for hypertension, including dosages and ○ Bradycardia (slow heart rate)
uses. ● Liver Function:
○ Methyldopa contraindicated in patients
Centrally Acting Alpha2 Agonists with impaired liver function
○ Periodic monitoring of serum liver enzymes
● Mechanism of Action: required
○ Decrease sympathetic response from the ● Rebound Hypertensive Crisis:
brainstem to peripheral vessels ○ Abrupt discontinuation can lead to rebound
○ Stimulate alpha2 receptors, leading to: hypertension; another antihypertensive
■ Reduced sympathetic activity should be prescribed if immediate
■ Increased vagal activity cessation is necessary
■ Decreased cardiac output ○ Symptoms of rebound hypertension include
■ Decreased serum levels of restlessness, tachycardia, tremors,
epinephrine, norepinephrine, and headache, and increased blood pressure
renin ○ Guanfacine has a lower risk of rebound
■ Reduced peripheral vascular hypertension
resistance and increased
vasodilation
● Cardiac and Renal Effects:
○ Minimal impact on cardiac output and renal ● Sodium and Water Retention:
blood flow ○ Can cause peripheral edema; diuretics may
● Drug Interactions: be prescribed with methyldopa or clonidine
○ Avoid with beta blockers due to risks of: to manage this
■ Enhanced bradycardia ● Pregnancy Considerations:
■ Rebound hypertension upon ○ Clonidine should be avoided during
discontinuation pregnancy
● Key Medications: ○ Methyldopa is often used for chronic or
○ Methyldopa: Early widely used pregnancy-induced hypertension but
antihypertensive; can cause sodium and crosses the placental barrier and may enter
water retention in high doses. breast milk
○ Clonidine: Available in a transdermal patch ● Patient Education:
for 7-day action; skin irritations may occur. ○ Emphasize adherence to prescribed
○ Guanfacine: Similar effects to clonidine; medication regimen.
long half-life, typically taken once daily.
● Combination Therapy:
○ Often administered with diuretics to
manage fluid retention.

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Alpha-Adrenergic Blockers significant blood pressure reduction and

reflex tachycardia.
○ Non Selective blockers are better for acute
● Mechanism of Action: hypertension; selective blockers are
○ Block alpha-adrenergic receptors, resulting preferred for long-term management.
in vasodilation and decreased blood ● Onset and Duration:
pressure. ○ Prazosin onset: 30 minutes to 2 hours;
○ Help maintain renal blood flow rate. duration: approximately 10 hours.
● Lipid Profile Benefits: ● Additional Information:
○ Decrease very-low-density lipoproteins ○ Table 44-2 contains drug data for selective
(VLDL) and low-density lipoproteins (LDL). and nonselective alpha blockers.
○ Increase high-density lipoprotein (HDL)
levels. SIDE EFFECTS AND ADVERSE REACTIONS
● Safety Profile:
○ Safe for patients with diabetes; do not ● Prazosin, Doxazosin, and Terazosin:
affect glucose metabolism or respiratory ○ Orthostatic hypotension (dizziness,
function. faintness, lightheadedness, increased heart
● Selective Alpha1-Blockers: rate, particularly with the first dose)
○ Examples: Prazosin, terazosin, doxazosin. ○ Nausea
○ Used mainly for hypertension and benign ○ Headache
prostatic hypertrophy. ○ Drowsiness
○ Prazosin is commonly prescribed; terazosin ○ Nasal congestion (due to vasodilation)
and doxazosin have longer half-lives and are ○ Edema
taken at bedtime. ○ Weight gain
● Drug Interactions: ● Phentolamine:
○ Prazosin can intensify hypotensive effects ○ Hypotension
when combined with alcohol or other ○ Reflex tachycardia (from severe blood
antihypertensives. pressure decrease)
● Sodium and Water Retention: ○ Nasal congestion (due to vasodilation)
○ Can cause edema; diuretics are often ○ Gastrointestinal disturbances
prescribed to mitigate fluid accumulation.
● Potent Alpha Blockers: Drug Interactions
○ Examples: Phentolamine,
phenoxybenzamine. General Interactions:
○ Used for hypertensive crises and severe
hypertension from catecholamine-secreting ● Interactions can occur with antiinflammatory drugs
tumors (pheochromocytomas). and nitrates (e.g., nitroglycerin).
● Pharmacokinetics:
○ Prazosin: absorbed via GI tract; significant
Specific Effects:
first-pass metabolism; short half-life
(requires twice daily dosing).
● Prazosin + Anti-Inflammatory Drugs:
○ Highly protein-bound; assess for adverse
○ Intensifies peripheral edema when taken
reactions when combined with other
daily.
protein-bound drugs.
● Prazosin + Nitroglycerin:
● Pharmacodynamics:
○ Risk of syncope (faintness) due to
○ Selective alpha blockers dilate arterioles
significant blood pressure decrease.
and venules, reducing peripheral resistance
and blood pressure.
○ Prazosin causes slight heart rate increase;
nonselective alpha blockers can lead to

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Adrenergic Neuron Blockers (Peripherally Cautions:

Acting Sympatholytics)
● Large doses may block beta2 receptors, increasing
Mechanism of Action: airway resistance.
● Not recommended for patients with severe asthma.
● Block norepinephrine release from sympathetic
nerve endings. Common Side Effects:
● Result in decreased cardiac output and peripheral
vascular resistance, leading to lower blood pressure. ● Orthostatic hypotension
● GI disturbances
Primary Drug: ● Nervousness
● Dry mouth
● Reserpine: Most potent adrenergic neuron blocker, ● Fatigue
used for severe hypertension. ● Large doses may cause AV heart block.

Side Effects: Direct-Acting Arteriolar Vasodilators

● Common: Orthostatic hypotension (advise patients Mechanism of Action:

to rise slowly).
● Vivid dreams, nightmares, and suicidal ideation may ● Direct-acting vasodilators relax smooth muscles of
occur with reserpine. blood vessels, primarily arteries, causing
● Sodium and water retention can happen, leading to vasodilation.
peripheral edema. ● Increase blood flow to the brain and kidneys.

Treatment Considerations: Effects:

● Considered the last choice for chronic hypertension ● Decrease blood pressure.
management. ● Can cause sodium and water retention, leading to
● Can be used alone or in combination with diuretics peripheral edema.
to manage edema.
Combination Therapy:
Alpha1- and Beta1-Adrenergic Blockers
● Diuretics can be administered alongside vasodilators
Mechanism of Action: to manage edema.

● Block both alpha1 and beta1 receptors. Key Medications:

● Example: Labetalol (Normodyne).
● Hydralazine and Minoxidil: Used for moderate to
Effects: severe hypertension.
○ Cause minimal orthostatic hypotension due
● Alpha1 Blockade: to limited arteriolar dilation.
○ Causes vasodilation, reducing resistance to ○ May induce reflex tachycardia and renin
blood flow. release due to vasodilation.
○ Stronger effect on alpha receptors lowers ○ Beta blockers are often prescribed to
blood pressure and moderately decreased counteract reflex tachycardia.
pulse rate.
● Beta1 Blockade: Emergency Use:
○ Decreases heart rate and atrioventricular
(AV) contractility. ● Nitroprusside: Used for acute hypertensive
emergencies.

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○ Very potent; rapidly decreases blood ● Primary Uses:

pressure affecting both arterial and venous ○ Treats hypertension.
vessels. ○ Effective in treating heart failure.
● Common ACE Inhibitors:
○ Benazepril (Lotensin)
Side Effects and Adverse Reactions ○ Captopril (Capoten)
○ Enalapril maleate (Vasotec)
Hydralazine: ○ Fosinopril (Monopril)
○ Lisinopril (Prinivil, Zestril)
● Reflex tachycardia ○ Moexipril (Univasc)
● Palpitations ○ Perindopril (Aceon)
● Edema ○ Quinapril (Accupril)
● Nasal congestion ○ Ramipril (Altace)
● Headache ○ Trandolapril (Mavik)
● Dizziness ● Guidelines:
● GI bleeding ○ Can be first-line antihypertensive therapy.
● Lupus-like symptoms ○ Thiazide diuretics recommended by JNC 7.
● Neurologic symptoms (tingling, numbness) ● Considerations:
○ Less effective in African Americans and
Minoxidil: older adults; often combined with diuretics.
○ Contraindicated in pregnancy (reduces
● Similar side effects to hydralazine placental blood flow).
● Tachycardia ○ Dose reduction necessary for renal
● Edema insufficiency (except for fosinopril).
● Excess hair growth ○ Most can be taken with food; moexipril
● Can precipitate an angina attack should be taken on an empty stomach for
efficacy.
Nitroprusside:
SIDE EFFECTS AND ADVERSE REACTIONS
● Reflex tachycardia
● Palpitations ● Common Side Effects:
● Restlessness ○ Constant, irritated cough (ACE cough).
● Agitation ○ Nausea.
● Nausea ○ Vomiting.
● Confusion ○ Diarrhea.
○ Headache.
Angiotensin-Converting Enzyme Inhibitors ○ Dizziness.
○ Fatigue.
● Mechanism of Action: ○ Insomnia.
○ Inhibit ACE → Reduces angiotensin II ○ Hyperkalemia (serum potassium excess).
(vasoconstrictor) formation. ○ Tachycardia.
○ Blocks aldosterone release → Decreases ● Management:
sodium retention and promotes potassium ○ ACE cough may resolve upon drug
retention. discontinuation.
● Effects: ○ ARBs can be used as alternatives without
○ Minimal change in cardiac output or heart cough.
rate. ● Major Adverse Effects:
○ Lowers peripheral resistance. ○ First-dose hypotension:
○ Useful for patients with elevated serum ■ More likely in patients on diuretics
renin levels. due to vasodilatory effects.

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○ Hyperkalemia: ○ Generally do not cause serum potassium

■ Elevated potassium levels can excess or loss.
occur. ● First-Line Treatment:
● Angioedema: ○ ARBs may be used as first-line therapy for
○ Swelling of face, tongue, lips, mucous hypertension.
membranes, and extremities.
○ Higher incidence in African Americans. Valsartan Specifics
○ May occur within hours to 1 week after the
first dose. ● Pharmacokinetics:
○ Can be reversed by discontinuing the drug. ○ Rapidly absorbed, undergoes first-pass
○ Laryngeal edema may require rescue metabolism in the liver.
epinephrine. ○ Highly protein-bound.
○ Half-life: 6 to 9 hours; duration of action:
CONTRAINDICATIONS ~24 hours.
○ Excreted in urine and feces.
Pregnancy: ● Pharmacodynamics:
○ Potent vasodilator; blocks angiotensin II
● Contraindicated due to potential harm to the fetus binding to AT1 receptors.
from reduced placental blood flow. ○ Peak effect: 4 to 6 hours.
● Efficacy:
Drug Interactions: ○ Less effective in treating hypertension in
African American patients.
● Avoid combining with potassium-sparing diuretics ○ Risk of angioedema similar to ACE
(e.g., spironolactone) to reduce hyperkalemia risk. inhibitors.
● Avoid salt substitutes containing potassium for the ● Administration:
same reason. ○ Can be taken with or without food.
○ Suitable for patients with mild hepatic
Angiotensin II Receptor Blockers insufficiency.

● Mechanism of Action: Direct Renin Inhibitor

○ Block angiotensin II from AT1 receptors →
Prevent aldosterone release. Approval:
○ Cause vasodilation and decrease peripheral
resistance. ● First FDA-approved direct renin inhibitor for
○ No cough side effects (unlike ACE hypertension.
inhibitors).
● Contraindications: Mechanism of Action:
○ Should not be used during pregnancy.
● Examples of ARBs: ● Binds with renin → Reduces levels of angiotensin I,
○ Losartan (Cozaar) angiotensin II, and aldosterone.
○ Valsartan (Diovan)
○ Irbesartan (Avapro) Effectiveness:
○ Candesartan cilexetil (Atacand)
○ Eprosartan (Teveten) ● Effective for mild and moderate hypertension.
○ Olmesartan medoxomil (Benicar) ● Can be used alone or with other antihypertensive
○ Telmisartan (Micardis) agents.
● Combination Products:
○ Losartan + hydrochlorothiazide (HCT)
○ Valsartan + hydrochlorothiazide (HCT)

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Combination Therapy: Reflex Tachycardia: Can occur with calcium blockers; more
prevalent with nifedipine.
● Has an additive effect when combined with thiazide
diuretics or ARBs. Pharmacokinetics: Amlodipine is highly protein-bound and
gradually absorbed via the GI tract.
Population Considerations:
Combination with Other Drugs:
● Less effective as monotherapy for blood pressure
reduction in the African American population. ● Beta blockers are generally not prescribed with CCBs
due to decreased myocardial contractility.
Calcium Channel Blockers ● CCBs lower blood pressure more effectively in
African Americans compared to other
antihypertensive categories.
Calcium Channels: Slow calcium channels are found in
myocardium and vascular smooth muscle (VSM) cells. SIDE EFFECTS AND ADVERSE REACTIONS

Effects of Calcium: Free calcium increases muscle Common Side Effects:

contractility, peripheral resistance, and blood pressure.
● Flushing
Calcium Channel Blockers (CCBs): ● Headache
● Dizziness
● Block calcium channels in VSM, promoting ● Ankle edema
vasodilation.
● Less effective on large central arteries compared to Serious Adverse Reactions:
coronary, cerebral, and peripheral vessels.
● Highly protein-bound with a short half-life; ● Bradycardia
slow-release forms reduce administration frequency. ● AV block
Drug Classes:

● Diphenylalkylamine: Verapamil (Calan) - treats

chronic hypertension, angina, dysrhythmias; acts on
arterioles and heart.
● Benzothiazepines: Diltiazem - similar uses as
verapamil.
● Dihydropyridines: Largest group; includes
amlodipine and others primarily for hypertension.
Nimodipine is used to prevent ischemic brain injury
from vasospasm after subarachnoid hemorrhage.

Specific Drugs:

● Nifedipine (Procardia): Lowers blood pressure in

older adults; associated with increased sudden
cardiac death in high doses (immediate-release
form). Sustained-release forms safer; used for acute
rises in hospital settings.
● Amlodipine (Norvasc): Long half-life, taken once
daily; may cause peripheral edema. Often combined
with ACE inhibitor benazepril (Lotrel).

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