Cardiovascular Medications Study Guide

NUR 3305 | Katie Knott, MSN, RNC-OB: Cardiovascular Medications

Week 7 Topics

  • Anti-hypertensives & Meds for Heart Failure

  • Diuretics & Anti-dysrhythmics

  • Anti-lipids, Anticoagulants, Antiplatelets & Thrombolytics

Cardiovascular System Overview

Student Learning Objectives

  1. Define key terminology relevant to medications that affect the cardiovascular system.

  2. Identify and explain how factors such as heart rate, stroke volume, contractility, preload, and afterload affect cardiac output.

  3. Identify normal and abnormal findings for adult blood pressure (BP) and heart rate (HR).

  4. Identify the management goals for patients diagnosed with hypertension, heart failure, and angina pectoris and which medications are first-line treatment for each.

  5. Identify mechanism of action, therapeutic effects, indications, side/adverse effects, drug interactions, and key considerations for anti-hypertensive and anti-anginal medications.

  6. Educate a patient on proper usage of nitroglycerin sublingual tablets/spray/powder.

Key Terminology

  • Cardiac output (CO): Volume of blood ejected from heart per minute, calculated as:
    CO=SV×HRCO = SV × HR
    where SV = stroke volume, HR = heart rate.

  • Inotropic: Refers to drugs affecting the force of cardiac contraction.

    • Positive inotropic agents: Increase contraction strength.

    • Negative inotropic agents: Decrease contraction strength.

  • Chronotropic: Refers to drugs affecting heart rate.

    • Positive chronotropic agents: Increase heart rate.

    • Negative chronotropic agents: Decrease heart rate.

  • Preload: The degree of stretch of the heart muscle before contraction.

  • Afterload: The resistance the heart must overcome to eject blood.

  • Contractility: The ability of cardiac muscle to contract.

  • Hypertension: Defined as elevated blood pressure greater than 130/80130/80.

  • Angina Pectoris: Sudden, sharp chest pain that can radiate to the left side.

Circulatory System

  • Primary Functions:

    • Deliver oxygen, nutrients, and electrolytes to cells via blood (systemic circulation).

    • Remove carbon dioxide and metabolic waste (pulmonary circulation).

  • Diastole: Defines the phase of the heartbeat when the heart muscle relaxes and allows the chambers to fill with blood.

  • Systole: Defines the phase of the heartbeat when the heart muscle contracts and pumps blood out of the chambers.

  • SA node: Acts as the pacemaker of the heart, generating 60-100 beats per minute (bpm).

  • AV node: Functions as a gatekeeper and backup pacemaker, establishing a rate of 40-60 bpm.

Blood Vessels

  • Arteries: Transport blood from the heart to tissues, branching into arterioles.

  • Capillaries: Serve as the site of fluid, oxygen, carbon dioxide, and nutrient exchange.

  • Venules: Collect blood from capillaries and transport it to veins, returning it to the heart.

  • Vessel Diameter: Determines the amount of peripheral resistance encountered.

Elements of Cardiac Output

  • Heart rate (HR): Controlled by the SA node.

    • Beta 1 (SNS): Increases HR (positive chronotropic).

    • Muscarinic (PSNS): Decreases HR (negative chronotropic).

  • Stroke Volume (SV): The volume of blood ejected from the left ventricle with each heartbeat.

  • Contractility: Strength of heart muscle contraction.

  • Venous Return: Impacted by blood volume and HR.

  • Preload: The initial stretching of cardiac muscle cells prior to contraction.

  • Afterload: The resistance the left ventricle must overcome to circulate blood.

  • Peripheral Resistance (PR): Determined by arteriole constriction/dilation.

  • The formula for cardiac output:
    CO=HR×SVCO = HR × SV

Regulatory Systems

  • Baroreceptor Reflex:

    • Baroreceptors located in the aortic arch respond to blood pressure changes.

    • When BP decreases, signals to the brain activate the sympathetic nervous system (SNS), which activates alpha 1 and beta 1 receptors, affecting vital signs (VS) and cardiac output (CO).

  • Kidneys & RAAS: Renin-Angiotensin-Aldosterone System (RAAS)

    • Renin is released in response to decreased glomerular filtration rate (GFR), leading to the formation of angiotensin I & II.

    • Angiotensin II induces vasoconstriction, promoting aldosterone release, which leads to sodium (Na) and water retention, increasing blood volume and peripheral resistance.

    • These mechanisms commonly oppose the therapeutic effects of antihypertensives.

Blood Pressure & Heart Rate

  • Blood Pressure (BP): Calculated as the product of cardiac output (COP) and peripheral resistance (PR).

  • Normal Parameters:

    • BP

    • HR (Reference: Burcham & Rosenthal, 2025, chap 50).

Hypertension Algorithm

  • Usage in Patient Care: Nurses and providers utilize algorithms to guide treatment decisions.

  • Considerations: Treatment often depends on the patient's age and associated co-morbidities; chronic management typically starts with a low dose and increases slowly.

  • In cases of hypertensive crisis or inpatient care, more aggressive treatment is necessary.

Heart Failure

  • Definition: A chronic disorder where the heart cannot pump sufficient blood to meet tissue demands, resulting in low cardiac output (COP).

  • Sympathetic Nervous System (SNS): Activates to increase heart rate, contractility, and vessel tone.

  • RAAS: Water retention contributes to heart stress.

  • Ventricular Dilation & Hypertrophy: Result from ongoing cardiac stress.

  • Primary Causes: Hypertension (HTN) and myocardial infarction (MI).

  • Compensatory Cycle: Can lead to increased morbidity and mortality (Reference: Burcham & Rosenthal, 2025, chap 51).

Heart Failure Management

  • Management Goal: Improve cardiac output and alleviate symptoms.

  • Medication Classes:

    • Diuretics

    • RAAS Inhibitors

    • Beta-blockers

    • Hydralazine

    • Inotropic agents: Digoxin, Dopamine.

Anti-hypertensives & Meds for Heart Failure

RAAS Inhibiting Drugs

  • Renin-Angiotensin-Aldosterone System (RAAS):

    • Regulates blood pressure, blood volume, and fluid/electrolyte balance. Activated when BP or blood volume is low (e.g., hemorrhage, anaphylaxis, shock).

    • Primary Purpose: Raise blood pressure.

  • Hormones and their Actions:

    • Renin: Released from kidneys in response to low BP, blood volume, or sodium.

    • Angiotensin I: Minor vasoconstriction, considered clinically irrelevant.

    • Angiotensin II: Causes significant vasoconstriction, increases blood pressure, promotes renal sodium retention.

    • Aldosterone: Promotes sodium retention and potassium excretion in kidneys, increasing blood volume and BP.

    • Antidiuretic Hormone (ADH): Released from pituitary, instructs kidneys to reabsorb water, thereby increasing blood volume and BP.

  • Implication: Both angiotensin II and aldosterone can contribute to detrimental cardiac remodeling, hypertrophy, and fibrosis.

Angiotensin-Converting Enzyme (ACE) Inhibitors

  • Drug Names: Captopril, Lisinopril (Zesteril, Qbrelis)

  • Mechanism of Action:

    • Suppress the formation of angiotensin II by blocking ACE and increasing bradykinin in the lungs.

  • Therapeutic Effects (Indication):

    • Vasodilation of arterioles and reduction of blood volume and BP, indicated for hypertension (HTN), heart failure (HF), myocardial infarction (MI), and diabetic nephropathy; protective against MI & HF.

  • Pharmacokinetics:

    • Excreted primarily via the kidneys.

  • Side / Adverse Effects:

    • Side Effects: First dose hypotension, persistent dry cough, hyperkalemia.

    • Adverse Effects: Renal failure, angioedema, neutropenia.

  • Interactions:

    • Diuretics intensify first dose hypotension (recommend cessation for 2-3 days prior).

    • Lithium level increases, NSAIDs diminish the effectiveness of ACE inhibitors.

    • Careful consideration required when administering with other antihypertensives; severe hypotension may occur if dosages are not adjusted accordingly.

  • Route(s): Oral (PO).

  • Other Considerations:

    • Use cautiously in patients with kidney disease; avoid in pregnancy.

    • Monitoring of BP, sodium, and fluid levels is essential.

Angiotensin II Receptor Blockers (ARBs)

  • Drug Names: Losartan (Cozaar), Valsartan (Diovan)

  • Mechanism of Action:

    • Directly block angiotensin II effects without affecting bradykinin.

  • Therapeutic Effects (Indication):

    • Similar to ACE inhibitors, this brings about vasodilation of arterioles, reduction of blood volume and BP, and serves as a second-line drug when ACE inhibitors are not tolerated.

  • Pharmacokinetics:

    • Information not provided in full detail but akin to ACE inhibitors.

  • Side / Adverse Effects:

    • Primarily angioedema and risk of renal failure.

  • Interactions:

    • Caution with other antihypertensives to avoid severe hypotension.

  • Route(s): Oral (PO).

  • Other Considerations:

    • Monitor BP, sodium, and fluid levels vigilantly; caution in patients with kidney disease and avoid in pregnancy.

Calcium & the Cardiovascular System

  • Calcium Channels: Located on vascular smooth muscle and linked to beta 1 receptors within the heart.

  • Action of Calcium:

    • In arteries and peripheral arterioles, calcium flow induces contraction triggered by action potentials.

    • In the heart, positive inotropic effects result in increased contraction force; SA and AV nodes experience enhanced contractility.

Calcium Channel Blockers
Diltiazem (Cardizem), Verapamil (Calan)

  • Mechanism of Action:

    • Prevent calcium ions from entering cardiac and arteriolar cells and block renin activity.

  • Therapeutic Effects (Indication):

    • Lower blood pressure & enhance perfusion, manage hypertension (HTN) and angina, slow ventricular rates in dysrhythmias (like A-fib/flutter), reduce automaticity & contractility.

  • Pharmacokinetics:

    • Metabolized hepatically.

  • Side / Adverse Effects:

    • Common reactions include constipation, dizziness, edema, flushing, and headaches due to vasodilation. Particularly concerning in older adults are papular/vesicular lesions, dyspnea, and depression.

    • Toxicity manifests as severe hypotension & cardiotoxicity (bradycardia, AV block).

  • Interactions:

    • Digoxin increases AV block risk; beta-blockers can lead to bradycardia (must be given hours apart); grapefruit juice can decrease metabolism and prolong effects.

  • Route(s): Available PO and IV.

  • Other Considerations:

    • Close monitoring of heart rate and BP is warranted, ongoing if administered IV. Caution is advised in patients with existing cardiac disorders.

Nifedipine (Procardia)

  • Mechanism of Action:

    • Prevents calcium ions from entering primarily arteriolar cells and blocks renin response.

  • Therapeutic Effects (Indication):

    • Similar effects as previously noted - decreased BP & enhanced perfusion for HTN, included angina; additionally can increase HR & force of contraction.

  • Pharmacokinetics:

    • Undergoes extensive first-pass metabolism.

  • Side / Adverse Effects:

    • Reactions include dizziness, edema, flushing, headaches, and, in older adults, papular lesions. There is a risk of reflex tachycardia which calls for combination use with beta-blockers (BBs).

    • Toxicity symptoms mirror other calcium blockers.

  • Interactions: No interactions specified.

  • Route(s): Available in oral formulations (IR, SR, XL).

  • Other Considerations:

    • Hemodynamically safer for patients with cardiac disorders although IR preparations carry increased risk. Monitoring of BP and HR before and after administration is critical.

Vasodilation

  • Effects:

    • Dilation of arterioles reduces cardiac afterload, increases cardiac output, and improves perfusion.

    • Dilation of veins decreases cardiac preload, reducing cardiac output and perfusion.

  • Indications for vasodilation include:

    • Hypertension / HTN crisis

    • Angina & myocardial infarction (MI)

    • Heart failure

    • Peripheral vascular disease (PVD)

Direct Vasodilators

  • Drug Names: Hydralazine (Apresoline)

  • Mechanism of Action:

    • Selectively dilates arterioles which decreases afterload.

  • Therapeutic Effects (Indication):

    • Used to decrease blood pressure (HTN & HTN crisis), short-term reduction of afterload in HF.

  • Pharmacokinetics:

    • Patient metabolism can vary genetically impacting the response; short half-life noted.

  • Side / Adverse Effects:

    • Common effects include headache, dizziness, weakness, and fatigue (due to vasodilation); risk of Na retention, orthostatic hypotension, fainting, and reflex tachycardia/HTN.

    • Acute rheumatoid syndrome can occur leading to muscle/joint pain, fever, and nephritis.

  • Interactions:

    • Other antihypertensives can cause severe hypotension when used with hydralazine.

  • Route(s): PO, IV.

  • Other Considerations:

    • Close monitoring of BP and HR is essential, especially if given IV. Often used in concert with beta-blockers and diuretics.

Angina Pectoris

  • Causes: Factors influencing angina include heart rate, contractility, preload, and afterload. Increased interaction among these raises oxygen demand on the heart.

  • Types: Includes stable (exertional) angina.

Antianginals

  • Drug Names: Nitroglycerin

  • Mechanism of Action:

    • Dilates veins, reduces preload, and decreases myocardial oxygen demand.

  • Therapeutic Effects (Indication):

    • Effective in reducing chest pain during acute angina episodes or as prophylaxis before exertion.

  • Pharmacokinetics:

    • Highly lipid soluble allowing for various administration routes; suffers extensive first-pass metabolism; short half-life of 5-7 minutes.

  • Side / Adverse Effects:

    • Commonly causes severe headaches, with tolerance development; reflex tachycardia may occur.

    • Risks of orthostatic hypotension, weakness, and flushing due to vasodilation.

  • Interactions:

    • Can cause severe hypotension when used with other antihypertensives or sildenafil (Viagra).

  • Route(s): Available in several forms including PO (sublingual, buccal, powder, spray), IV, transdermal patches, and topical applications.

  • Other Considerations:

    • Monitoring of BP and HR is crucial; tolerance to nitroglycerin can develop over time.

Nitroglycerin Usage Instructions

  • Refer to Lexi-Drug for the patient education sheet on nitroglycerin SL tablets/powder.

  • Important considerations include:

    • Where/how to administer.

    • Situations when to take the medication.

    • Recommended waiting period between doses.

    • Actions to take if angina symptoms persist.

Antianginals – Other Medications

  • Beta-Adrenergic Blockers:

    • Example medications and their mechanism of action (MOA) effectiveness for angina must be discussed.

  • Calcium Channel Blockers:

    • Example medications and their effectiveness in the management of angina must be reviewed.

References

  • Burcham, J. R. & Rosenthal, L. D. (2025). Lehne’s Pharmacology for Nursing Care (12th ed.). Elsevier.

  • Horn, J. R., Hansten, P. D. (2013). Diuretics, ACEIs, ARBs and NSAIDs: A nephrotoxic combination. Allergy & Asthma, 79(4). Diuretics, ACEIs, ARBs, and NSAIDs: A Nephrotoxic Combination | Pharmacy Times.