Pharmacology Exam 3 Study Guide: Cardiac Drugs, Exams of Pharmacology

This study guide covers cardiac drugs, including heart failure medications, antihypertensives, and antianginals. It details the mechanisms of action for various drug classes such as ace inhibitors, arbs, beta blockers, and calcium channel blockers. It also includes information on side effects, contraindications, drug interactions, and nursing implications, providing a comprehensive review for pharmacology students. The guide also covers first-line therapies for angina and hypertension in pregnancy, along with protocols for administering nitroglycerin and preventing drug tolerance. (410 characters)

Typology: Exams

2025/2026

Available from 12/27/2025

mindshaper
mindshaper 🇺🇸

1.3K documents

1 / 14

Toggle sidebar

This page cannot be seen from the preview

Don't miss anything!

bg1
Pharmacolog
y Exam 3 Study
Guide
Cardiac Drugs – Heart Failure, Antihypertensives, Antianginals, Etc.
(NOT Antidysrhythmic)
1. MOA of each class of cardiac drugs, i.e., how do beta blockers work? how do calcium
channel blockers work? etc. (Don’t forget page 27 in your packet –
Antihypertensives)
ACE Inhibitors [MOA]
Inhibits Angiotensin Converting Enzymes [ACE]
ACE is Responsible for Converting Angiotensin I to Angiotensin II
Angiotensin II (2 – TWO)
POTENT Vasoconstrictor AND Stimulator of Aldosterone
Aldosterone Stimulates Sodium/Water Reabsorption AND
Stimulates Excretion of K+ as well
Angiotensin II Blockers [ARBs][MOA]
Allows Angiotensin II to be Made BUT Blocks the Receptor Sites for it to Bind
Prevents Vasoconstriction and Prevents Secretion of Aldosterone
ARBS = POTENT VASODILATORS
Direct Renin Inhibitors [MOA]
Binds with Renin
Inhibits Conversion of Angiotensinogen into Angiotensin I
Approved ONLY for Hypertension
Aldosterone Antagonists [MOA]
Blocks Receptors for Aldosterone
Indicated for Hypertension and Heart Failure (in Severe Stages)
Beta Blockers [MOA][ -LOL, -OLOL]
Cardioprotective Quality
Prevents Catecholamine-Mediated Actions on the Heart by
Reducing/Blocking SNS Stimulation to the Heart and the
Heart’s Conduction System
Decreases Cardiac Output and HR
B-Type Natriuretic Peptides [VASODILATORS][MOA]
pf3
pf4
pf5
pf8
pf9
pfa
pfd
pfe

Partial preview of the text

Download Pharmacology Exam 3 Study Guide: Cardiac Drugs and more Exams Pharmacology in PDF only on Docsity!

Pharmacolog

y Exam 3 Study

Guide

Cardiac Drugs – Heart Failure, Antihypertensives, Antianginals, Etc.

(NOT Antidysrhythmic)

  1. MOA of each class of cardiac drugs, i.e., how do beta blockers work? how do calcium

channel blockers work? etc. (Don’t forget page 27 in your packet –

Antihypertensives)

  • ACE Inhibitors [MOA]

▪Inhibits Angiotensin Converting Enzymes [ACE]

▪ACE is Responsible for Converting Angiotensin I to Angiotensin II

▪Angiotensin II (2 – TWO)

▪POTENT Vasoconstrictor AND Stimulator of Aldosterone

▪Aldosterone Stimulates Sodium/Water Reabsorption AND

Stimulates Excretion of K+ as well

  • Angiotensin II Blockers [ARBs][MOA]

▪Allows Angiotensin II to be Made BUT Blocks the Receptor Sites for it to Bind

▪Prevents Vasoconstriction and Prevents Secretion of Aldosterone

▪ARBS = POTENT VASO DILATORS

  • Direct Renin Inhibitors [MOA]

▪Binds with Renin

▪Inhibits Conversion of Angiotensinogen into Angiotensin I

▪Approved ONLY for Hypertension

  • Aldosterone Antagonists [MOA]

▪Blocks Receptors for Aldosterone

▪Indicated for Hypertension and Heart Failure (in Severe Stages)

  • Beta Blockers [MOA][ -LOL , - OLOL ]

Cardioprotective Quality

▪Prevents Catecholamine-Mediated Actions on the Heart by

Reducing/Blocking SNS Stimulation to the Heart and the

Heart’s Conduction System

▪Decreases Cardiac Output and HR

  • B-Type Natriuretic Peptides [ VASODILATORS ][MOA]

▪Vasodilator Effects on BOTH Arteries and Vein=Decreases Preload

AND Afterload

  • Phosphodiesterase Inhibitors [MOA]
  • Inhibiting the Enzyme Phosphodiesterase
  • Milrinone (ONLY Available Phosphodiesterase Inhibitor Drug)
  • Cardiac Glycosides [MOA]

▪Positive Inotropic

o Inhibits Na+/K+ Pump

o Allows More Calcium to Stay in the Cardiac Cell

o Increases Myocardial Contractility

o Increased Force and Velocity of Myocardial Contraction (Without an Increase

in Oxygen Consumption)

▪Negative Chronotropic

o Suppresses the SA Nodes (Decreases Heart Rate)

▪Negative Dromotropic Effect

o Decreased Automaticity at SA Node

o Decreased AV Nodal Conduction

  • Calcium Channel Blockers [- DIPINE ][MOA]

▪PRIMARY USE: Hypertension AND Angina

▪Prevents Muscle Contractions

▪Blocks the Binding of Calcium which Causes the Smooth Muscle to Relax

▪Promotes Dilation of the Arteries

NO EFFECT on HEART

▪EXCLUDING Verapamil and Diltiazem

▪Promotes Cardiosuppression

▪Used for Hypertension, Angina, AND Dysrhythmias

  1. What drugs/classes are first line therapy for angina? (remember NBC)
    • FIRST Line Therapy for ANGINA ( NBC )

N itrates [Nitrites]

B eta Blockers

C alcium Channel Blockers [CCBs

  1. What are prodrugs? Which ACE inhibitors are not prodrugs? What is the significance of this?
    • Prodrugs

▪Drugs that are NOT ACTIVE UNTIL they reach the Liver

▪They Become Active when Metabolized (Metabolite)

  • ACE Inhibitors

▪Captopril (Capoten) and Lisinopril (Prinivil) ARE NOT PRODRUGS !!!!!!

▪IMPORTANT Because these Drug Do NOT Need to Reach the Liver

to Become Active

  1. Common SE of ACE inhibitors, ARBs, calcium channel blockers, beta blockers, nitrates
    • ACE Inhibitors [Side Effects]

▪FIRST DOSE PHENOMENON [First-Dose Syncope]=First Dose

  • Angiotensin II Receptor Blockers [ARBs][Side Effects]

▪UTI

Angioedema

▪Headache, Dizziness, Fatigue

▪Renal Failure=Occurs in Patients with Bilateral Renal Artery

▪Do NOT Produce Cough

▪May Cause Mild Hyperkalemia

▪Toxicity Manifests with Decreased BP and Increased Pulse

o Potent Vasodilators (↓BP, ↑ Pulse)  Reflex Tachycardia

  • Beta Blockers [Side Effects]

▪CNS: Fatigue, Dizziness, Depression

▪Cardiac: Bradycardia , CHF, Orthostatic Hypotension

▪Respiratory: Bronchospasms, Dyspnea (SOB)

▪GI: N/V, Diarrhea, Colitis, Constipation

▪GU: Decreased Libido and Impotence

▪Endocrine: Blocks Normal Symptoms of Hypoglycemia

  • Nitrates [Side Effects]

o P roteinuria (Increased Level of Protein in Urine)

o O rthostatic Hypotension (MAJOR)

o R enal Failure/ R ash

o L iver Toxicity/ L eukopenia (Form of

Agranulocytosis)

o A ngioedema (Swelling of the Lips, Tongue, Throat)=Allergic

Reaction

o T aste Changes [Dysgeusia]

o P ruritis

o I ncreased K+ (Especially with Potassium-Sparing Diuretics)

▪-DIPINE Group [Side Effects]

o Dizziness, Facial Flushing, Headache, Peripheral Edema (Ankles/Feet)

ALL the Result of Vasodilation

o GI: CONSTIPATION (Major)

o Gingival Hyperplasia (Overgrowth of the Gums)

o Hypotension

o Exacerbation of HF

o Causes Bradycardia

  • Calcium Channel Blockers [CCBs][Side Effects]

➢ Mild = Calcium Channels Blockers [CCBs]

➢ Severe = STOP CCBs

o Reflex Tachycardia

o Partial or Complete AV

Block

o Eczematous Skin Eruptions In the Elderly

▪Verapamil and Diltiazem [Side

Effects]

Headaches

o Intensity/Frequency Diminishes with Continued Use

o Wear Gloves when Applying Patch or Paste

o May Treat with Acetaminophen

▪Reflex Tachycardia

▪Postural (Orthostatic) Hypotension

▪ALL THREE ABOVE EFFECTS are caused by VASODILATION

▪Tolerance May Develop

  1. What may occur if beta blockers are stopped abruptly? Abrupt Discontinued Use of

Beta Blockers can Result in Increased INTENSITY of Angina OR MI (Heart Attack)

  1. What is reflex tachycardia? Heartbeat Caused by a Variety of Autonomic Nervous

System Effects

  1. Why are beta blockers administered to treat reflex tachycardia? Effects (Change in BP,

Fever, Emotional Stress

  • Nursing Implications

▪Monitor BP and Apical Pulse [AP]

▪HOLD Diuretics 1 WEEK Prior to Starting ACE Inhibitors

▪Can Cause FETAL HARM

▪Interactions

▪NSAIDs (Decreases Antihypertensive Effects)

▪Lithium (Monitor for Toxicity [>1.5])

▪Potassium-Sparing Diuretics (Hyperkalemia)

▪Antihypertensive and Diuretics (Causes Additive Effect)

  1. Nitrates drug of choice (DOC) for exertional angina (angina of effort, classic angina),

acute anginal attacks (nitroglycerin)

  • Nitrates

▪DOC for Exertional angina [Chronic Stable Angina] (Effort

Angina, Classic Angina)

▪DOC for Acute Anginal Attacks (Specifically Nitroglycerin)

  1. Nitroglycerin has large first pass effect – what does this mean? How does it affect dosage?
    • Nitroglycerin

▪Has a LARGE First Pass Effect=Means Drug Dosage is

GREATLY REDUCED by the Liver when Ingested and Dosage

Needs to Be Increased

  1. Know contraindications for and drug interactions with nitrates (especially drugs for ED)
    • Nitrates [Nursing Contraindications]

o Causes Absorption to be More Gradual and Effective

▪Administer IV Forms with Extreme Caution ( ALWAYS Use an IV Pump )

▪Remind Patient that Medication is Only Part of Therapy

o Patients Should Manage Diet, Stress Level, Weight, Alcohol Intake

▪Instruct Patients to Avoid Smoking and Eating Foods High in Sodium

▪Encourage Supervised Exercise

▪Teach Patient to Change Positions Slowly

o Performed to Avoid Syncope from Postural Hypotension

▪Instruct Patients to Report Unusual Shortness of Breath, Dyspnea,

Swelling of the Feet/Ankles/Around the Eyes, Weight Gain/Loss, Chest

Pain, Palpitations, Excessive Fatigue

Male Patients who Take These Drugs May NOT Be Aware of that

Impotence is an Expected Side Effect (Inform them of Side Effect)

o This May Influence Compliance with Drug Therapy

▪If Patient is Experiencing Serious Adverse Effects OR Believe the

Dose/Med Needs to be Changed, They Should Contact Their

HPC IMMEDIATELY

▪Things that Can Lower BP (Leads to Fainting + Injury)

o Hot Tubs, Showers, or Baths

o Hot Weather

o Prolonged Sitting/Standing

o Physical Exercise

o Alcohol Ingestion

▪Patient Should Sit/Lie Down Until Symptoms of Dizziness Subside

▪Patients SHOULD NOT Take Other Meds Without Getting Approval from HPC

▪ ]

o Causes Vasodilation AND Lowers

BP

-DIPINE Group [Side Effects

o NO EFFECT on HEART

o Promotes Dilation of the Arteries

  • Calcium Channel Blockers [- DIPINE ]

Smooth Muscle to Relax

  1. What are the differences in the two groups of calcium channel blockers? Know the MOA

▪-DIPINE Group [MOA]=PRIMARY USE: Hypertension AND

Angina o Prevents Muscle Contractions=Blocks the Binding of Calcium which Causes the

and SE of both groups

o Gingival Hyperplasia (Overgrowth of the Gums)

o Dizziness, Facial Flushing, Headache, Peripheral Edema (Ankles/Feet)

➢ ALL the Result of Vasodilation

o Eczematous Skin Eruptions In the Elderly

➢ Mild = Calcium Channels Blockers [CCBs]

o GI: CONSTIPATION (Major)

➢ Severe = STOP CCBs

  • Verapamil and Diltiazem [MOA]

o Promotes Cardiosuppression

o Used for Hypertension, Angina, AND Dysrhythmias

o Blocks Calcium Channels in Vascular Smooth Muscle AND THE HEART

o PROMOTES CARDIOSUPPRESSSION

Dilation of Arterioles ( Decreases BP )

➢ Increases Coronary (Heart) Perfusion

Decreases Heart Rate

➢ Decreases AV Nodal Conduction

➢ Decreases Force of Contraction

▪Verapamil and Diltiazem [Side Effects]

o Hypotension

o Partial or Complete AV Block

o Exacerbation of HF

o Causes Bradycardia

  1. Monitor urine output for patients on cardiac drugs (what is minimal acceptable

urine output per hour?)

  • Minimal Acceptable Urine Output PER Hour

▪ 30 ml Per Hour

  1. What to do for Patients receiving IV cardiac meds?
    • IV Cardiac Meds

▪Patients SHOULD BE MONITORED for the First Couple of

Hours (Minimum) When Receiving IV CARDIAC MEDS

  1. What are first-line drugs for heart failure? (see heading on Heart Failure handout)

st

Line Drugs for Heart Failure

▪Loop Diuretics

▪ACE Inhibitors

▪Angiotensin II Receptor Blockers [ARBs]

▪Beta Blockers

  1. Nursing implications for administering digoxin; what is positive inotropic and

negative chronotropic?

  • Digoxin [Nursing Considerations]

▪ NOTHING TO BP!! (NOT A CARDIOVASCULAR DRUG)

Does Digoxin is taken Once Per Day

o If MISSED, it can be Taken No More than 12 Hours After Passed

Scheduled Time

Antilipemic (Cholesterol Lowering) Drugs

  1. Desired levels of total cholesterol, HDL, LDL, VLDL, and triglycerides (Cholesterol

is ONLY FOUND IN ANIMAL PRODUCTS)

  • Total Cholesterol

▪200mg or LOWER

▪Limit Fat Intake; Limit Cholesterol Intake to Less than 300mg/day

  • HIGH-Density Lipoproteins ( THE GOOD STUFF )(RECYCLES Cholesterol)

▪60mg or HIGHER (HIGHER = REMOVES ONE RISK FACTOR)

▪Can INCREASE Value with EXERCISE

  • LOW-Density Lipoproteins [LDL]

▪LESS THAN 130

▪LESS THAN 100 (FOR CAD Patient’s)

  • VERY LOW-Density Lipoproteins [VLDL]

▪LESS THAN 130

▪DIET Can LOWER This Value

  • Triglycerides

▪LESS THAN 150

▪Increases with Diabetes Mellitus [DM] and Pancreatitis

  1. Risk factors for CAD
    • Cholesterol Levels of 300 mg/dL

▪Three to Four Times Greater than Patients under 200 mg/dL

  • Obesity, Diabetes, High BP, Stroke, Peripheral Heart Disease
  • Physical Inactivity, Smoking, Age, Gender, Family History
  1. Which class of drug is best for lowering total cholesterol?
  • DOC for Lowering Total Cholesterol

▪-STATINs

  1. When (what time of day) are statins administered? With or without food? Why?
    • -STATINs Should be Taken in the EVENING

▪Take with 6 – 8 oz of Water

▪Food is Recommended to Decrease GI Distress

▪Lovastatin REQUIRES to be Taking with The EVENING MEAL

o “I LOVE My EVENING MEAL”

  1. Statins – contraindicated for alcoholic liver disease; acceptable for non-alcoholic

liver disease

  • -STATIN [Contraindications]

▪ALCOHOLIC Liver Disease

o It is OKAY for NON-ALCOHOLIC Liver Disease

  1. What labs to check prior to and throughout statin drug use
    • LFTs Are Check Before AND During Use of - STATINs
  2. SE for each class of antilipemics
    • HMG-CoA Reductase Inhibitor (- STATIN )[Side Effects]

▪Mild, Transient Gastrointestinal (GI) Disturbances (MOST COMMON)

o Constipation (MOST COMMON), Dyspepsia [Heart

Burn], Cramps, Flatulence

▪Rash

▪Headache

▪Peripheral Vasodilation

▪Myopathy [Muscle Pain]

Hepatotoxicity (CHECK LFTs)

  • Cholesterol Absorption Inhibitors [Ezetimibe (Zetia) – ONLY CAI]
  • Bile Acid Sequestrants [SE](SAFEST Drugs for Lowering Cholesterol)[SE]

▪Not Absorbed from GI Tract

▪NO Systemic Side Effects (SAFEST)

▪Constipation

▪Heartburn [Dyspepsia], Nausea, Belching, Bloating

o These May Increase Triglycerides

o Disappear Over Time

o Food Decreases GI Distress

o Increased Fiber (Fiber Supplements [Psyllium] Work as well)

➢ Relieves Constipation and Bloating

  • Fibric Acid Derivatives [Fibrates][- FIBR - Can Be Found in Names][SE]

▪Ex. Feno FIBR ate

DIARRHEA (THINK: “Fiber” will Produce Diarrhea)

o Only Fibrates Cause Diarrhea

▪Blurred Vision, Headache

▪Increased Risk of Gallstones

▪Prolonged Prothrombin Time (PT)

▪Liver Studies may Show Increased Enzyme Levels

  • Niacin [Nicotinic Acid][Side Effects]

▪Intense Flushing (Caused by Histamine Release)

▪Pruritus

▪GI Distress

▪Liver Injury (Hepatotoxic)

▪Vasodilation (Related to Prostaglandin and Histamine)

o Small Dose Aspirin and Other NSAIDs 30 Minutes Before Niacin

➢ May Help Cutaneous Flushing and Itching

o Due to Bile Acid Sequestrants Not Being Absorbed

o TREATMENT = Restoring Gut Motility

▪Drug Interactions

o ALL Drugs Must be Taken 1 Hour BEFORE OR 4 – 6 Hours AFTER

➢ Avoids Decreased Absorption of the Other Drugs

o High Doses of BAS Decrease Absorption of Fat-Soluble Vitamins

➢ Fat-Soluble Vitamins [A, D, E, K]

o Thiazide, Diuretics, Digoxin, Warfarin, and Some Antibiotics

  • Fibric Acid Derivatives [Fibrates][Interactions]

▪Oral Anticoagulants (INCREASES Risk of Bleeding)

▪STATINS (Increases risk of Rhabdomyolysis, Myalgias, and Myositis)

  • Niacin [Nicotinic Acid][Interactions]

▪Niacin + - STATINs

o Increases Risk of Myopathy

▪Niacin + Antihypertensives

o Further Lowers BP (Vasodilation)

▪Contraindication in Patients with Increased Serum Uric Acid (Ex. Gout)

  1. SE of niacin (nicotinic acid) and how to treat these
    • Niacin [Nicotinic Acid][Side Effects]

▪Intense Flushing (Caused by Histamine Release)

▪Pruritus

▪GI Distress

▪Liver Injury (Hepatotoxic)

▪Vasodilation (Related to Prostaglandin and Histamine)

o Small Dose Aspirin and Other NSAIDs 30 Minutes Before Niacin

➢ May Help Cutaneous Flushing and Itching

▪Take with or After Meals (Decreases GI Side Effects)

▪Symptoms Usually Decrease After 2 Weeks of Therapy

  1. Patient teaching for antilipemic agents
    • Before Beginning Therapy

▪Obtain a Thorough Health/Medication History

  • Assess Dietary Patterns, Exercise Level, Weight, Height, Vital Signs, Tobacco

and Alcohol Use, and Family History

  • Assess for Contraindications, Conditions that Require Cautious Use, Drug Interactions

▪Includes Biliary Obstruction, Liver Dysfunction, Active Liver Disease

  • Obtain Baseline Liver Function Studies
  • Patients on Long-Term Therapy May Need Supplemental Fat-Soluble Vitamins

▪Fat-Soluble Vitamins [A, D, E, K]

  • Refer to Guidelines Regarding Administration Times and Meals
  • Counsel Patient Concerning Diet and Nutrition on an Ongoing Basis
  • Powder Forms MUST Be Taken with a Liquid, Mixed Thoroughly (and

Gently), and NEVER TAKEN DRY

▪Can Cause Esophageal Irritation If Swallowed Dry

  • Other Drugs Should be Taken 1 Hour BEFORE OR 4 – 6 Hours AFTER BAS

▪Avoids Interference with Absorption of Other Drugs

  • Start Niacin on Low Initial Dose and Gradually Increase it (+ Take with Meals)

▪Helps Minimize Adverse Effects of Niacin

  • Small Doses of Aspirin or NSAIDs may be Taken 30 Minutes BEFORE Niacin

▪Helps Minimize Cutaneous Flushing

▪Acetaminophen (Tylenol) Is NOT AN NSAID!!!!

  • Provide Teaching Regarding Use of NSAIDs and Aspirin
  • Inform Patients that These Drugs may Take Several Weeks to Show Effectiveness
  • Instruct Patients to Report Persistent GI Upset, Constipation, Abnormal

or Unusual Bleeding, and Yellow Discoloration of the Skin

  • Monitor for Therapeutic Effects

▪Reduced Cholesterol and Triglyceride Levels

o Specifically Decreased Total Cholesterol, LDL, Triglycerides

o Increase in HDL (THE GOOD STUFF)

  • -STATINs Are CATEGORY X DRUGS!!!!

▪Inform Patient to Notify HCP if Pregnancy is Planned/Expected

  • Antilipemic Agents are HIGHLY PROTEIN BOUND
  • Food is Recommended when Taking -STATINs to Decrease GI Distress
  • Recommend Patient to Take Antilipemic Drugs in the Evening

▪Cholesterol is Synthesized (Produced) Between 12am [Midnight] – 5am

  • Fibrates are PRIMARILY Affect Triglycerides

▪Can Lower Total Cholesterol/LDL and Raise HDL

Dosage Calculations – to include:

  1. IV drip rates (mL/hr, gtt/min., etc.); know that on an infusion device (pump) you

must calculate for an hour – know how to do this even if something ordered for less

than an hour

  1. Calculate dosages and weight-based calculations, including heparin bolus

and drip/infusion rates