NURS 2113 - Medications Module 5&6

Statins (HMG-Co-A Reductase Inhibitors) examples

Lipitor (atorvastatin)

Crestor (rosuvastatin)

Zocor (simvastatin)

Bile Acid-binding resins examples

Olestyr (cholestyramine)

Nicotinic Acid examples

Niacin (vitamin B3)

Nitrates Mech Of Action

converting to nitric oxide (NO) in the body, which activates guanylate cyclase, increasing cyclic GMP (cGMP) in smooth muscle cells, leading to lower intracellular calcium, muscle relaxation (vasodilation), and reduced oxygen demand in the heart

Nitrates effect on the Cardiovascular system

VASODILATION

• Venodilation: dilate veins, reducing venous return to the heart (preload). decreases volume of blood heart must pump, lowering myocardial oxygen demand

• Arterial Dilation: At higher doses, reduces systemic vascular resistance (afterload)

• Coronary Artery Dilation: Improve blood flow to the heart muscle by dilating coronary arteries and enhancing collateral circulation

Nitrates Relief of Angina

• Reduces both preload and afterload = decreased myocardial oxygen demand

• Improved coronary blood flow enhances oxygen supply to the heart, relieving chest pain

Nitrates Nursing Considerations

• Monitor therapeutic response

• Educate patients

CONSIDERATIONS FOR VASODILATION:

• Monitor for hypotension

• assess for headaches

• Check for reflex tachycardia: Monitor the patient’s pulse and consider beta-blockers if prescribed to counteract this effect

Nitrates Patient Education

• Teach patients to take sublingual at the onset of chest pain and to call emergency services if pain persists after the first dose.

• Instruct patients to store in their original container, away from light and moisture, to maintain potency.

Nitrates Therapeutic Effect

Decrease the frequency and severity of angina episodes

Nitrates examples

Nitrostat, Nitro-Dur (nitroglycerin)

Antiplatelet Classes

• Aspirin: Most common

• Clopidogrel (Plavix): used in combination with aspirin for dual antiplatelet therapy.

• Phosphodiesterase Inhibitors

• Glycoprotein IIb/IIIa Inhibitors

Aspin Mech of Action

Inhibits the enzyme cyclooxygenase-1 (COX-1), which reduces the production of thromboxane A2. This prevents platelets from becoming sticky and aggregating

Glycoprotein IIb/IIIa Inhibitors mech of action

Block the glycoprotein IIb/IIIa receptor that forms bridges between platelets and facilitate their aggregation at sites of vascular injury. Blocking these receptors prevents fibrinogen from binding. This disrupts platelet aggregation and thrombus formation, reducing the risk of arterial occlusion

Phosphodiesterase Inhibitors mech of action

Increase levels of cyclic AMP (cAMP) in platelets, reducing their ability to aggregate

Clinical applications of Glycoprotein IIb/IIIa Inhibitors Thrombolytic

Primarily used in conditions where platelet aggregation plays a critical role, such as:

• Acute Coronary Syndromes (ACS): Unstable angina or non-ST elevation myocardial infarction (NSTEMI).

• Percutaneous Coronary Interventions (PCI): To prevent thrombotic complications during angioplasty or stent placement.

Glycoprotein IIb/IIIa Inhibitors Thrombolytic nursing considerations

• Monitor for Bleeding

• Have reversal agents (Retavase, Streptokinase, Alteplase, Tenecteplase) or supportive measures (platelet transfusion) readily available

• MUST BE GIVEN WITHIN 1 HOUR AFTER START OF HEART ATTACK SYMPTOMS

Pharmacological treatment Options for Heart Failiure

• Phosphodiesterase inhibitors (PDE3 inhibitors)

• Beta blockers (beta adrenergic antagonists)

• Cardiac glycosides

• Angiotensin-converting enzyme inhibitors (ACEIs)

• Angiotensin receptor blockers (ARBs)

• Diuretics

Phosphodiesterase Inhibitors (PDE3 Inhibitors) examples

Primacor (milrinone)

Phosphodiesterase Inhibitors (PDE3 Inhibitors) Mech of action

Normally, the PDE3 enzyme breaks down cAMP in heart and vascular cells. PDE3 inhibitors block this enzyme, allowing cAMP to accumulate, which leads to stronger heart contractions (positive inotropy) and relaxation of blood vessels (vasodilation) by increasing calcium influx and activating protein kinases

Phosphodiesterase Inhibitors (PDE3 Inhibitors) Effects

• Higher cAMP levels boost the heart's pumping strength by increasing calcium levels in the heart muscle. This makes each heartbeat stronger, positive inotropic effect. (heart can pump more blood to meet the body’s needs)

• Improved blood flow

Cardiac Glycosides examples

Lanoxin (digoxin)

Cardiac Glycosides Indication

• heart failure

• certain arrhythmias

Cardiac Glycosides mechanism of action

• Inhibition of Na+/K=-ATPase pump: blocking this pump, intracellular sodium levels increase, disrupting the normal sodium gradient

• Impact on calcium: increased intracellular sodium reduces the activity of the sodium-calcium exchanger, which normally removes Ca+ from the cell. intracellular calcium accumulates. This calcium is released during each heartbeat, leading to stronger cardiac muscle contractions (positive inotropic effect)

• Slower Heart Rate: Cardiac glycosides enhance vagal tone, which slows conduction through the atrioventricular (AV) node. This results in a negative chronotropic effect (slower heart rate) and helps control arrhythmias like atrial fibrillation.

Cardiac Glycosides therapeutic effects

• Increased cardiac contractility that improves cardiac output,

• Slowing the heart rate allowing for better ventricular filling and more efficient blood circulation

Cardiac Glycosides (Digoxin) nursing considerations

• Monitor for Toxicity: narrow therapeutic window. Signs of toxicity include nausea, vomiting, visual disturbances (e.g., yellow-green halos), and arrhythmias.

• Check Apical Pulse: measure the apical pulse for one full minute before administering. Hold medication if pulse is below 60 beats per minute in adults.

• Renal Function: excreted by kidneys, impaired renal function can lead to drug accumulation and toxicity. Adjust doses accordingly.

Digoxin

• The most widely used cardiac glycoside, derived from the foxglove plant (Digitalis purpurea).

• Used for heart failure and atrial fibrillation.

Cardiac Glycosides (Digoxin) patient education

• Signs of toxicity (nausea, vomiting, visual disturbances (e.g., yellow-green halos), and arrhythmias

• Importance of adhering to prescribed doses.

• Avoid over-the-counter medications that may interact with cardiac glycoside (NSAIDS, ANTACIDS, COUGH MEDS

What to do if Cardiac Glycosides (digoxin) toxicity occurs

Digoxin immune fab (Digibind) can be administered IV to rapidly neutralize digoxin

***toxicity has made this drug the THIRD line of treatment with ACEI’s being the first line.