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Cardiovascular Pharmacology: An In-
Depth Briefing
I. Drugs for Heart Failure
Heart failure (HF) is a condition where the heart muscle weakens, enlarges, and loses its ability to pump blood effectively. This can lead to blood backing up into the lungs (left- sided HF) or peripheral tissues (right-sided HF). Pharmacological treatment aims to improve the heart's pumping efficiency and manage symptoms.
Cardiac Glycosides: Digoxin
Digoxin is a cornerstone drug for treating heart failure and certain dysrhythmias like atrial fibrillation. It is derived from the foxglove plant and has a powerful, multifaceted effect on heart muscle. Mechanism of Action: Digoxin inhibits the sodium-potassium pump in cardiac cells. This leads to an increase in intracellular sodium (sodium inside cell), which in turn allows an influx of calcium. This increased calcium causes the cardiac muscle fibers to contract more efficiently.
- Flooding cell with calcium is key to the 3 defining therapeutic effect Three Core Effects on the Heart:
- Positive Inotropic: Increases the force and efficiency of myocardial contraction. ; makes heart pump stronger and significantly boosts cardiac output and improving blood flow throughput body
- Negative Chronotropic: Decreases the heart rate.
- Negative Dromotropic: Decreases the conduction of heart cells.; particulary as it goes through AV node **Together, these actions:
- Increase cardiac output**
**2. improve blood flow, decrease edema
- promote fluid excretion by the kidneys. Memory Aid: The "S-P-S" Action of Digoxin** Remember Digoxin's effects by thinking it makes the heart S-P-S :
- S tronger (Positive Inotropic)
- P aced (slower rate - Negative Chronotropic)
- S lower in conduction (Negative Dromotropic)
Drug interactions
- Diuretics
- Glucocorticoids
- Antacids
- Herbal interactions Digitalis Toxicity: Due to a narrow therapeutic window, toxicity is a significant risk, can.
- Anorexia, nausea, vomiting, diarrhea, halos around lights, tinnitus
- Bradycardia, dysrythmias, visual disturbance
- Therapeutic Level: 0.5 to 2.0 ng/mL
- If renal function decline or taking other drug that interacts, toxicity level can spike
- Signs & Symptoms: o Gastrointestinal: Anorexia, nausea, vomiting, diarrhea o Cardiac: Bradycardia, premature ventricular contractions, cardiac dysrhythmias o Neurologic: Headaches, malaise, confusion, delirium o MOST SPECIFIC Visual: Blurred vision, visual illusions (white, green, or yellow halos around objects), ringing in the ears (tinnitus)
- Key Risk Factor: Hypokalemia (low potassium) significantly increases the risk of digoxin toxicity.
- Antidote: Digoxin immune Fab (Digibind) binds with digoxin to form complex molecules that are then excreted in the urine. Nursing Considerations:
Diuretics First-line treatment to reduce fluid volume and edema. Beta Blockers Improve cardiac performance over time; doses are started low and gradually increased.; vessel opens so blood can pump better, like calcium blockers Vasodilato rs Decrease venous blood return (preload) and reduce the force the ventricle pumps against (afterload). Phosphodi esterase Inhibitors
- (e.g., Milrinone Lactate) Promote a positive inotropic response and vasodilation. Used for acute HF
- Increase stroke volume, cardiac output, and vasodilation
- Inhibit enzyme phosphodiesterase
- Caution administered IV for no longer than 48-72 hours to avoid severe dysrhythmias; high alert med Inotropics Causes blood to pump hard; slow down hard and causes heart to pump harder to pump out more blood
II. Antihypertensive Drugs Hypertension is defined as a systolic pressure >140 mm Hg or a diastolic pressure >90 mm Hg. Treatment involves a multi-pronged approach to reduce blood volume, decrease systemic vascular resistance, and regulate cardiac output. ; vasodilators Memory Aid: Drug Suffixes for Antihypertensives A simple way to identify major antihypertensive drug classes is by their common suffixes:
- Beta-Blockers end in - LOL
- ACE Inhibitors end in - PRIL
- Angiotensin Receptor Blockers: ARBs end in - SARTAN
- Alpha-Blockers end in – SIN
- Diuretics
- Beta Adrenergic Blockers
- Central Acting Alpha 2 Agonist
- Some Calcium Channel Blockers end in - PINE
Diuretics
Diuretics promote sodium and water loss, decreasing fluid volume and thus lowering blood pressure. Diuretic Type Site of Action Key Effects & Considerations Thiazide Diuretics (e.g., Hydrochlorothiazi de) Distal Convoluted Tubule Promotes Na+, K+, and Mg+ excretion. Promotes Ca+ reabsorption (can cause hypercalcemia). Not for patients with severe renal dysfunction. Loop Diuretics (e.g., Furosemide) Loop of Henle Most potent diuretics. Cause loss of Na+, K+, Mg+, and Ca+. Can increase renal blood flow. Preferred for patients with reduced creatinine clearance. Potassium- Sparing Diuretics (e.g., Spironolactone) Collecting Duct / Late Distal Tubule Weaker diuretic. Promotes Na+ and water excretion while retaining K+. Risk of hyperkalemia , especially if given with ACE inhibitors. Memory Aid: Diuretic Electrolyte Effects
- Loop diuretics make you lose everything (K+, Na+, Ca++, Mg++).
- Thiazide diuretics save Calcium.
- Potassium-Sparing diuretics obviously save Potassium.
Sympatholytics (Beta-Adrenergic Blockers)
Mechanism of Action: Beta-blockers reduce cardiac output by diminishing the sympathetic nervous system's response. They block catecholamines (epinephrine, norepinephrine), which decreases heart rate, contractility, and renin release.
- Non-selective Beta-Blockers (e.g., Propranolol): Inhibit both beta-1 (heart) and beta-2 (lungs) receptors. Can cause bronchoconstriction and are contraindicated in patients with COPD.
Angiotensin II Receptor Blockers (ARBs) Mechanism of Action: Block angiotensin II from binding to its receptors, preventing vasoconstriction and the release of aldosterone.; Dilate venules and arterioles, reducing afterload and preload, and improving renal blood flow
- ARBs are less effective for African Americans adults and older aduts with monotherapy Memory Aid: "-SARTAN" Spares the Cough
- ARBs end in - SARTAN (e.g., Losartan, Valsartan).
- They work similarly to ACE inhibitors but do not cause the irritating cough , making them a common alternative. Think of a "Sar-tan" to relax your vessels without the irritation. ; Other side effects include dizziness, drowsiness, blurred vision, head ache, diarrhea, insomnia
Calcium Channel Blockers (CCBs)
V ery N ice D rugs: V erapamil, N ifedipine, D iltiazem Mechanism of Action: Block calcium channels in the vascular smooth muscle, promoting vasodilation and decreasing blood pressure.; decrease contractility cause congestive heart failure
- Examples: Nifedipine, Verapamil, Diltiazem, Amlodipine.
- Side Effects: Headache, flushing, dizziness, peripheral edema, bradycardia, decreased blood pressure
- Nursing Intervention: Avoid grapefruit juice, which can intensify the drug's effect.
- Contraindications: congestive heart failure
Centrally Acting Alpha 2 Agonist
Mechanism of Action: stimulate the alpha 2 receptors= decrease in sympathetic activity Contraindications: impaired liver function Side Effects: sodium and water retention (can cause swelling in lower extremities), dry mouth, bradycardia
- Diuretics are frequently prescribed to avoid fluid retention
- Avoid abruptly stopping the drug, can cause rebound hypertension
Alpha-Adrenergic Blockers
Mechanism of Action: Block alpha-1 adrenergic receptors, resulting in vasodilation and decreased blood pressure. Memory Aid: "-SIN" to Relax
- Alpha-blockers end in - SIN (e.g., Doxazosin, Prazosin). Blocking alpha is no " sin " for lowering BP.
- A major side effect is orthostatic hypotension.; other is nasal congestion, edmea, weight gain, headache, nausea
Direct Acting Antihypertensive Drugs
Action: direct acting arteriolar vasodilators- used in extreme cases
- Diazoxide, hyrdalazine, minoxidil, nitroprusside Side Effects: reflex tachycardia, palpitations, restlessness, agitation, confusion, hyperglycemia
III. Antianginal Drugs Angina pectoris is acute cardiac pain caused by inadequate (or low) blood flow and oxygen to the myocardium. Antianginal drugs work by increasing oxygen supply or decreasing oxygen demand.
Nitrates: Nitroglycerin
- Understand if it’s stable angina (aware that chest pain will occur before doing a task) or unstable angina (Chest pain while relaxing), cardiac status is worst if occurring while at rest) Generate Hypothesis
- Patient will state anginal pain has decreased or they can effectively treat it if it appears; not a pain medicine but kow that it adequately dilates vessels for effective perfusion; stops the issue that CAUSES the pain Take Action
- Monitor vital signs
- Position the patient lying down or sitting when administering for first time because it decreases blood pressure and the client can become dizzy
- Monitor effects of IV nitroglycerin: headache, low BP, chest pain Evaluate Outcome
IV. Antidysrhythmic Drugs Antidysrhythmics are used to restore normal cardiac rhythm. They are categorized into four main classes based on their mechanism of action. Class Mechanism of Action Key Drugs Mentioned Class I: Sodium Channel Blockers Sodium Channel Blockers; effect sodium that goes into that Krebbs cycle that’s going to cause heart to beat 1A, 1B,1C: decrease the influx of ions, stabilizing membranes, change the rhythm of how heart beats Lidocaine, Quinidine Class II: Beta- Adrenergi c blockers Beta-Adrenergic Blockers, does the same thing as sodium channel blockers but just on the beta receptor sites Propranolol, Metoprolol, Atenolol
Class III Drugs that Prolong Repolarization-resting negative charge after contracting (Potassium Channel Blockers) Amiodarone Class IV Calcium Channel Blockers Verapamil, Diltiazem Memory Aid: "Some Body Peeled Carrots" This phrase helps remember the drug class actions in order:
- S ome - > S odium (Class I)
- B ody - > B eta-blockers (Class II)
- P eeled - > P otassium (Class III)
- C arrots - > C alcium (Class IV) Nursing Care
- Obtain baseline vitals and EKG to validate if the heart rhythm is normal or not
- Establish IV access
- Obtain cardiac enzymes (tell us if client if client is having MI), chemistry panels, liver and kidney function, drug toxicology Clinical Judgement Concept
- Perfusion Recognize cues
- Obtain baseline vital signs ECG for future comparison: if abnormal make sure to see if it’s normal to client Analyze cues and prioritize hypothesis
- Descreased tissue perfusion, dysrhythmia Generate Solutions
- Patient will have normal sinus rhythm Take Action
- Monitor vitals
- Monitor ECG for abnormal findings EVERYDAY
- Tell patient to report side effects to HCP
- Advise patient to avoid alcohol, caffeine, and tobacco because they cause vasodilation and make sure client rhythm stay normal Evalutate Outcomes
Bile Sequestrants
- Reduces LDL levels by binding with bile acids in the intestines
- Cholestyramine (questran), Colestipol (cloestid)
- Side effects : Constipation, flatulence (gas) , cramping
Fibric Acid
- Reducing triglycerides and VLDL levels, not effective in lowering LDL levels o gemfibrozil, (Lopid) ;fenofibrate (Tricor, Fibricor, Lofibra).
- Contraindications: anticoagulants-causes bleeding
- Monitor kidney function tests
- May cause gall stones in long term use.
- Use with caution when given with a statin- can cause muscle damage and statin toxicity due to poor elimination of drugs.
Nicotinic Acid
- Niacin, Vit B
- Reduces VLDL and LDL
- Has numerous side effects: diarrhea, confusion, tongue redness, facial flushing & peeling.
- Large doses required (not many patients tolerate)
- Available OTC
Cholesterol Absorption Inhibitor
- Acts on cells in the small intestine to inhibit absorption of cholesterol
- Increased excretion of cholesterol from GI tract
- Reduced LDL, triglycerides
- Usually combined with
VI. Drugs Affecting Coagulation These medications are used to prevent or dissolve clots. It is critical to differentiate their actions.
Drug Type Mechanism of Action Primary Use Anticoagulan ts Inhibit clot formation Venous thrombosis (DVT, PE) Antiplatelets Prevent platelet aggregation Arterial thrombosis (MI, Stroke) Thrombolytic s Dissolve existing clots ("clot busters") Acute MI, Ischemic Stroke, PE
Anticoagulants and Their Antidotes
Anticoagulant Key Information Lab Monitoring Antidote Heparin Fast-acting (IV, SubQ). Binds with antithrombin III. aPTT Protamine Sulfate Low-Molecular-Weight Heparin (LMWH) (e.g., Lovenox) Lower risk of bleeding. No routine monitoring needed. None Protamine Sulfate Warfarin (Coumarin) Slow-acting (Oral). Inhibits hepatic synthesis of Vitamin K. PT / INR Vitamin K Direct Thrombin Inhibitors (e.g., Dabigatran) Inhibit thrombin directly. aPTT (for some) Idarucizu mab Direct Factor Xa Inhibitors (e.g., Rivaroxaban, Apixaban) Inhibit Factor Xa. None required Andexanet alfa Memory Aids: Anticoagulation Facts
- H eparin H its fast; W arfarin W aits to work.
- For labs: You measure H eparin with aPTT ; you measure W arfarin with PT.
