Cardiovascular Medications Overview

Cardiovascular Drugs - Module 7

• Heart medications manage arrhythmias, angina (chest pain), blood pressure, cholesterol, and blood clots.

Acute Coronary Syndrome (ACS)

• ACS is a spectrum of clinical presentations related to acute myocardial infarction (NSTEMI & STEMI) and angina (stable & unstable [UA]).
• In ACS, a plaque in a coronary artery ruptures or erodes, triggering the clotting cascade.
• This leads to blood clot formation, obstructing the artery and interrupting blood/oxygen flow to cardiac muscle.

Plaque Formation

• Atherosclerosis occurs when plaque forms within the artery wall.
• The plaque narrows the artery lumen.

Lipid Deposition

• Lipid deposition is a key contributing factor to plaque formation.
• Endothelial injury is a site where lipid deposition occurs.

Thrombus formation

• A thrombus is a blood clot.
• Formation occurs frequently in damaged areas like the plaques in the artery walls.

Platelet Adhesion

• Platelets adhere to the damaged endothelium, forming a clot.

Embolus Formation

• An embolus is a thrombus dislodged and transported to a distant site.
• Blocking blood vessels downstream could have serious consequences.

Occlusion Causes Infarction

• Occlusion (blockage of a blood vessel) leads to tissue infarction.
• Collateral flow may try to compensate.

ACS Management

• Initial Care: ABCs, supplemental oxygen (if O2 saturation < 94%), IV access, monitor vitals, pulse oximetry, blood pressure, SAMPLE history (past medical history), assess discomfort (rated 0-10), 12-lead ECG, reperfusion checklist (start if no contraindications), aspirin, nitroglycerin, morphine.
• 12-Lead ECG Evaluation: Evaluate for injury, ischemia, or normal ECG patterns.
• Reperfusion Strategy: Different strategies for STEMI, UA/NSTEMI.
• Medications: Beta blockers, Clopidogrel, Heparin, ACE inhibitors, statins (oral), reperfusion medication is determined, and further steps are implemented as needed based on 12-lead ECG results.

ACS Drugs

• MONA: Acronym used for medications administered during ACS treatment are given in this order: Oxygen, Morphine, Nitroglycerin, Aspirin.
• Order of administration can differ.

Oxygen

• Administered if oxygen saturation is below 94%.

Aspirin

• Standard dosages for treating ACS are 160-325mg chewable aspirin.
• Speeding up absorption is a key advantage of the chewable form.
• Aspirin inhibits platelet aggregation, reducing further occlusion risk.

Nitroglycerin

• Used for treating chest pain from ACS.
• Given sublingually via spray or rapidly dissolving tablet.
• Dose repeated every 5 minutes if the first dose does not reduce pain (no maximum dose); use with continuous monitoring of blood pressure.
• Also relaxes vascular smooth muscle, improves blood flow to ischemic areas, and lowers myocardial oxygen consumption.

Morphine

• Administered for pain relief in ACS situations.
• Dose is 2.5mg, repeated every 5 minutes intravenously, and the maximum dose is 10mg.
• It's an opioid acting primarily on pain receptors.
• Also a venodilator, reducing ventricular preload and cardiac oxygen requirements.
• Blood pressure must be monitored continuously.
• If hypotension occurs, elevate the patient's legs and give intravenous fluids as ordered, and monitor for symptoms of pulmonary congestion.

Antihypertensive Drugs

• Different classes of drugs used to manage high blood pressure, including alpha1 blockers, beta blockers (names often end in '-lol'), ACE inhibitors (names often end in '-pril'), Angiotensin receptor blockers (names often end in '-sartan'), calcium channel blockers (names often end in '-pine'), diuretics, and vasodilators.

Alpha1 Blockers

• Drugs like doxazosin (Cardura), prazosin (Minipress), and terazosin (Hytrin) stimulate or block alpha receptors, leading to hypertension or hypotension.

Beta Blockers (Class II)

• These drugs block beta receptors in the heart, which are linked to calcium channels.
• This action reduces calcium influx, which is crucial for automaticity.
• Beta blocking decreases calcium influx and decreases automaticity and AV conduction.
• Drug examples: propranolol (Inderal), acebutolol (Sectral), esmolol (Brevibloc).

ACE Inhibitors

• Drugs like captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil/Zestril), quinapril (Accupril), ramipril (Altace), benazepril (Lotensin), and fosinopril (Monopril) block the conversion of angiotensin I to angiotensin II.
• Angiotensin II is a potent vasoconstrictor; blocking it lowers blood pressure.

Renin-Angiotensin-Aldosterone System (RAAS)

• Angiotensin II is a potent vasoconstrictor increasing blood pressure and stimulating aldosterone release.
• ACE inhibitors block this system, resulting in decreased blood pressure.

Aldosterone

• Aldosterone promotes sodium and water reabsorption in the kidneys, increasing blood volume and therefore preload.
• By blocking ACE, this effect is reduced by ACE inhibitors, reducing blood volume and preload.

Calcium Channel Blockers (Class IV)

• Drugs like verapamil (Calan), diltiazem (Cardizem), and nifedipine affect the heart's calcium channels, reducing automaticity, AV conduction, and myocardial contractility. Reduced blood pressure & used in treating angina and tachycardia.

Diuretics

• Diuretics promote urination, reducing excess fluid buildup in the body.
• These drugs can be important for people with heart failure to prevent fluid accumulation (lungs, abdomen, legs, ankles, feet).
• Diuretics reduce workload by reducing preload by reducing blood volume.

Diuretic Classes

• Thiazides, such as chlorothiazide (Diuril) and hydrochlorothiazide (HCTZ/HydroDIURIL).
• Loop diuretics, such as furosemide (Lasix) and bumetanide (Bumex).
• Potassium-sparing diuretics, such as spironolactone (Aldactone).

Antihyperlipidemic Drugs

• Medications to manage cholesterol and prevent fatty plaque buildup in blood vessels (arteries).

Cholesterol Metabolism

• Cholesterol is a vital component of cell membranes and hormone production, and necessary for proper function.

Lipoproteins

• Lipoproteins transport cholesterol (carried with proteins to make them soluble.)
• LDLs carry most cholesterol in the body and are considered 'bad' cholesterol because they deposit in the body vessels.
• HDLs carry cholesterol back to the liver and are considered 'good' cholesterol.

Why We Fear Cholesterol

• High LDL levels contribute to the development of coronary artery disease (CAD) and its associated complications like heart attacks and strokes—causing the narrowing of arteries, reducing blood/oxygen supply and causing harm to tissues.
• Damaged or oxidized LDL deposits under endothelial cells.
• Activated macrophages engulf oxidized LDLs, leading to foam cell formation.
• Foam cells contribute to plaque formation and narrowing of arteries.

Antihyperlipidemic Agents

• HMG-CoA reductase inhibitors (statins) reduce LDL synthesis in the liver, increase LDL receptors, and lower LDL levels to reduce the risk of re-infarction( recurrence of a heart attack).

Antiplatelet Agents

• Medications like aspirin reduce platelet aggregation.
• Clopidogrel (Plavix) inhibits platelet function to reduce the formation of clots.
• Platelet aggregation is a key step in clot formation.

Glycoprotein IIb/IIIa Inhibitors

• These drugs, such as abciximab and others, are strong platelet inhibitors by preventing the receptor site on platelets from connecting to other platelets during the aggregation process.

Anticoagulants

• Unfractionated heparin and low-molecular-weight heparin (LMWH) like enoxaparin (Lovenox) inhibit thrombin to prevent clot formation.
• Heparin prevents fibrin formation and inhibits platelet activation.
• Unlike some other medications, there's no direct reversal agent for LMWH.
• Agents like warfarin and protamine are used to reverse their anticoagulant effects. Different mechanisms are involved in reversing the effects of the agents.

Heparin

• A natural anticoagulant released by mast cells/basophils.
• It enhances the action of antithrombin III, an enzyme to inactivate thrombin, to stop clotting.
• Its mechanism of action involves binding to antithrombin III, which enhances antithrombin's ability to inactivate thrombin to stop clot formation.

Warfarin (Coumadin)

• Warfarin reduces the production of vitamin K-dependent clotting factors such as II, VII, IX, and X to stop clot formation.
• Its effects take time to develop (~12 hours).

Fibrinolytics/Thrombolytics

• Reperfusion therapy is used in situations where reperfusion (restoration of blood flow) is critical
• These drugs dissolve blood clots in arteries and veins for emergency situations.

tPA (tissue plasminogen activator)

• tPA is a fibrinolytic drug (enzyme) that directly breaks down clots to restore blood flow.
• tPA enhances the activation of plasminogen to break down clots.

Occlusion Mechanism

• Occlusion (blockage) results in a thrombus or embolus stopping blood flow.