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NU578 Exam 7 Class Discussion, Lecture notes of Nursing

University of South Alabama (USA)Nursing

Discussion of Exam 7 in class notes

Typology: Lecture notes

2024/2025

Uploaded on 06/11/2025

caroline-ngo 🇺🇸

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Drugs for Heart Failure

Digoxin (Lanoxin) : cardiac glycoside

oIncreases cardiac contractility (+inotropic effect) by inhibiting Na-K ATPase (increases Ca

entry into cell) increase CO (does not correct remodeling)

oDecreases HR

oDecrease AB nodal conduction

oPharmacokinetics:

Good PO absorption, but tablets <capsules

Don’t switch dosage forms

Dosage is based on lean body weight. It is 70% renally excreted, so good renal

function is important

Therapeutic digoxin levels: 0.5-0.8 ng/ml

oAdverse Reactions:

*Anorexia, N/V/D, confusion, blurred vision (halos), *Arrhythmias

Dig toxicity is made much worse by *hypokalemia or anything that decreases

clearance

oTreatment for Toxicity: d/c dig, correct K+, administer Digibind (antibodies to dig that

pull it out of circulation)

oDrug interactions (many)

Quinidine : displaces dig from tissues, decreases dig excretion, decreases dig

dose when using quinidine

Antacids: bind dig and decrease absorption

Diuretics: cause hypokalemia and increase toxicity

oMore harm than good in females

ACE Inhibitors for CHF : First-Line treatment for CHF

oIn CHF, CO is ↓. As a result, blood flow to kidneys is ↓. In response, the kidneys release

renin which converts angiotensinogen (a plasma protein) to angiotensin 1. Angio 1 is

converted to angiotensin II by ACE in the lungs.

o Angio II plays a major role in maintaining fluid balance in the body (it also worsens CHF)

by acting as a vasoconstrictor (↑ pre + afterload), and by stimulating the release of

aldosterone from the adrenal cortex. Aldosterone increases Na + H20 retention, ↑ blood

volume, ↑ pre- + afterload.

oAdverse Reactions

COUGH

Hyperkalemia, dizziness, angioedema

oAlso used for HTN

oCaptopril, Enalapril, Lisinopril, Fosinopril, Quinapril

oRamipril and Trandolapril—approved for HF post MI

oACEI—not in acute decomp HF

Prolong life, dilate arterioles and veins, suppress aldosterone release, favorable

impact on cardiac remodeling with prolonged use (ARBS less favorable here)

Other Treatment Strategies for CHF

oDiuretics (help with fluid imbalance)—always used

Partial preview of the text

Download NU578 Exam 7 Class Discussion and more Lecture notes Nursing in PDF only on Docsity!

Drugs for Heart Failure

 Digoxin (Lanoxin): cardiac glycoside o Increases cardiac contractility (+inotropic effect) by inhibiting Na-K ATPase (increases Ca entry into cell) increase CO (does not correct remodeling) o Decreases HR o Decrease AB nodal conduction o Pharmacokinetics:  Good PO absorption, but tablets <capsules  Don’t switch dosage forms  Dosage is based on lean body weight. It is 70% renally excreted, so good renal function is important  Therapeutic digoxin levels: 0.5-0.8 ng/ml o Adverse Reactions:  *Anorexia, N/V/D, confusion, blurred vision (halos), *Arrhythmias  Dig toxicity is made much worse by *hypokalemia or anything that decreases clearance o Treatment for Toxicity: d/c dig, correct K+, administer Digibind (antibodies to dig that pull it out of circulation) o Drug interactions (many)  Quinidine : displaces dig from tissues, decreases dig excretion, decreases dig dose when using quinidine  Antacids: bind dig and decrease absorption  Diuretics : cause hypokalemia and increase toxicity o More harm than good in females  ACE Inhibitors for CHF : First-Line treatment for CHF o In CHF, CO is ↓. As a result, blood flow to kidneys is ↓. In response, the kidneys release renin which converts angiotensinogen (a plasma protein) to angiotensin 1. Angio 1 is converted to angiotensin II by ACE in the lungs. o Angio II plays a major role in maintaining fluid balance in the body (it also worsens CHF) by acting as a vasoconstrictor (↑ pre + afterload), and by stimulating the release of aldosterone from the adrenal cortex. Aldosterone increases Na + H20 retention, ↑ blood volume, ↑ pre- + afterload. o Adverse Reactions  COUGH  Hyperkalemia, dizziness, angioedema o Also used for HTN o Captopril, Enalapril, Lisinopril, Fosinopril, Quinapril o Ramipril and Trandolapril— approved for HF post MI o ACEI—not in acute decomp HF  Prolong life, dilate arterioles and veins, suppress aldosterone release, favorable impact on cardiac remodeling with prolonged use (ARBS less favorable here)  Other Treatment Strategies for CHF o Diuretics (help with fluid imbalance)—always used

 Thiazide diuretics if renal function is good o Cardiac stimulants like Dobutamine (Dobutrex), Milrinone (Primacor) in short term tx o Vasodilators (drugs for HTN)  BiDil—hydralazine/isosorbide dinitrate o Sometimes Beta Blockers to reduce cardiac work and help in remodeling  Carvedilol (Coreg), Bisoprolol (Zebeta), Metoprolol (Toprol XL) improve LV EF, slow progression of HF, decrease hospi9talizations when added to regiment  May take up to a month to show improvement o Combination therapy common - digoxin or ACEI + thiazide diuretic. This ↑ contractility, ↓ TPR, ↓ Na + H20 load.  Nitrates: reduce afterload and sometimes both preload and afterload o Nitroglycerin: relieves pulmonary edema  Venous vasodilator o Sodium Nitroprusside: venous and arteriolar vasodilator  Increases afterload and reduces pulmonary edema  Profound hypotension o Nesiritide (Natrecor): a BNP derivative  Indicated for short term IV tx in patients with dyspnea at rest and increase PCWP  Suppresses RAAS, creases pre and afterload, decreases central sympathetic outflow  Outcome is long lasting vasodilation and enhanced sodium and water excretion  Dose 48 hours or less, symptomatic hypotension or renal compromise are indications to stop  Inotropic Agents: o Dopamine : Short term rescue measure for acute HF  Activates b1 receptors in the heart increasing CO, increases renal blood flow and UOP  Activates a1 receptors increasing vasoconstriction—a disadvantage o Dobutamine : only works on b1 receptors to increase CO and contractility
 Phosphodiesterase Inhibitors: o Inamrinone : increases contractility and causes vasodilation (an inodilator)  2-3 day IV treatment for acute HF who have not responded to diuretics, RAAS inhibitors, and digoxin  Constant monitoring o Milrinone : as above  Drugs to AVOID in HF o Antidysrhythmic Drugs  Are cardio suppressive  Amiodarone (Cordarone) and Dofetilide (Tikosyn) do not adversely affect survival o CCVs  Worsen HF  Vasoselective CCVs (Nifedipine and Amlodipine) do not reduce survival o NSAIDS

Centrally-Acting Sympathetic Agonists Peripherally Acting Sympathetic Antagonists Beta Blockers

Peripheral Arterial Vasodilators Arterial Venous Vasodilators Calcium Channel Blockers

Antiarrhythmic Drugs

Treatment of Angina Pectroris

 3 main types: o Stable: CP caused by exercise or stress o Unstable: more severe than stable; may develop at rest and cause myocardial damage o Variant (Prinzmetal’s): due to vasospasm of coronary vessels; may occur at rest, same time each day  Drug therapy increase O2 to heart (vasodilators) or decrease cardiac O2 consumption (BB)  Nitroglycerine and CCBs used for all types of angina  Long-acting nitrates used for unstable, variant prophylaxis  B-blockers used for stable, unstable  • Warnings/Contraindicated in tachycardia, (>100 bpm), bradycardia (<50), systolic hypotension, R ventricular infarct. Concomitant Sildenafil or Vardenafil (24h) or Tadalafil (48 hrs) Drug Selection for Angina:  BB: good for HTN, migraine, DM, vascular disease, CHF, valvular disease  CCB: good in cardiac conditions such as dysrhythmias, depression, asthma/COPD Useful Educational Tools for Patients with ACS and CAD

o Lepirudin (Refludan): Used IV to treat clots in patients with heparin-induced thrombocytopenia. o Argatroban (Acova): IV to treat clots in HIT o Desirudin (Ipravask): subQ for DVT o Warfarin: DVT, PE, heart valves  Monitor PT or INR. Want INR 2-3. The average Prothrombin time is 12 sec. With warfarin on board, the PT is LONGER. How much longer? It is compared to a PT standard used in the lab where the patient is tested. On warfarin, the PT time should be 1.3-1.5 times LONGER (hence the value 1.3-1.5—your patient should take LONGER to clot while on the drug). But…because the PT each lab uses is different, the INR—international normalized ratio-- is now used in most labs. This takes into account the different PT preps. For most patients, an INR of 2-3 is used. When you monitor patients using the INR, it will “look” like they take about twice as long to clot while taking warfarin.  Antidote: phytonadione (vitamin K)  Fibrinolytics:  Antiplatelets:  Other drugs with effects on bleeding o DTI

 Desirudin (Iprivask)  Bivalrudin (Angiomax)  Argatroban (Argatroban) Dabigatran (Pradaxa)  Lepirudan (Refludan)  These are indicated for Stroke, HIT, and DVT prophylaxis

 Administer all anti HLD drugs at night except for atorvastatin  New statin SE: hepatotoxicity, myopathy, do NOT use in pregnancy, confusion  Statins do not prevent early death or a first cardiac event – Statins may cause muscle weakness – Statins may increase diabetes risk by 28% – Statins MAY affect cognition

NU578 Exam 7 Class Discussion, Lecture notes of Nursing

Related documents

Partial preview of the text

Download NU578 Exam 7 Class Discussion and more Lecture notes Nursing in PDF only on Docsity!

Drugs for Heart Failure

Treatment of Angina Pectroris