NRSG 2700 unit 9

heart failure and myocardial infarction

Nonpharmacologic treatment of cardiovascular disease

decrease alcohol and high fat and high cholesterol foods, keep lipid labs and bp in normal range, keep blood glucose in normal range, exercise regularly, maintain healthy weight, don’t use tobacco

MI/Angina treatment

reduce frequency of episodes, improve exercise tolerance, participate in ADLs to extend lifespan, primarily done by decreasing cardiac oxygen demand

Nitroglycerine class and MOA

organic nitrate, forms nitric oxide which results in the release of calcium ions in the smooth muscle (relaxes arterial and venous smooth muscle, decreases myocardial oxygen demand, and directly dilates coronary arteries and decreases spasms)

Nitroglycerine TE

relief of angina pain and IV (IV is used to maintain hen during surgery, treatment of HF, acute pulmonary edema, and HTN emergency)

Nitroglycerine con

htn, head injury w increased ICP

Nitroglycerine SE

headache, flushing, OH, syncope, reflex tachycardia

Nitroglycerine inter

use w phosphodiesterase-5 inhibitors and may cause severe htn and cardiovascular collapse, ctn w other antihypertensive meds, sympathomimetics will antagonize effects

Nitroglycerine NC/T

be aware of many forms, avoid getting ointment on skin, tolerance to Nitroglycerine is common and serious, monitor vs, supervise ambulation, w angina take 1 tab SL and if pain is not relieved then take up to 3 tabs at 5-min intervals (max 3 in 15min), apply transdermal patch at same time daily, store in original container, rest for 15 minutes after taking and change positions slowly

HF pump failure

cardiac output is too low to meet the bodys needs

HF factors

atherosclerosis, mitral stenosis, chronic HTN, diabetes, myocardial infarction is the #1 cause of HF

Heart failure can be ____ or _____ sided

right, left

The body works hard to compensate for cardiac dysfucniton with

ventricular hypertrophy, cardiac remodeling, SNS activation, and activate RAAS system

S/S of HF

dyspnea at rest or on exertion, fatigue, palpitations, angina

Right sided HF has

JVD and pedal edema

Left sided HF has

pulmonary edema and cough

Treatment objectives of HF

increases effectiveness of the heart and decreases the workload of the heart

Stages of HF

1. No s/s during activity

2. Slight limitations during activity

3. Marked limitations during activity

4. Activity intolerant and s/s at rest

3 goals of pharmacotherapy with HF

1. Reduce preload

2. Increase contractions

3. Reduce after load

ACE inhibitors goal

lower bp and decrease blood volume. Ends in “pril”

ARBs goal

also known as receptor blockers, they lower bp and decrease blood volume. End in “sartan”

Diuretics goal

decrease blood volume and lower bp

Beta antagonists goal

slow heart rate, decrease bp, reverse cardiac remodeling

Vasodilators goal

lower bp

Cardiac glycosides

not a first line med and is used for late-stage HF. Used by ancient people for poison arrows. Increases strength of cardiac contraction

Phosphodiesterase 3 inhibitors

not used often, only for acute and decompensated HF. Action is similar to dobutamine but lasts longer. Increases the strength of cardiac contraction and causes vasodialtion

Atenolol class and MOA

beta adrenergic antagonist, blocks beta 1 receptors in the heart and slows rate and reduces contractility

Atenolol TE

decreases myocardial oxygen demand, reduces cardiovascular mortality and MI prophylaxis, treats stable angina, treats HTN

Atenolol con

severe hypotension. Don’t use for severe bradycardia, decompensated HF, stroke, CKD

Atenolol SE

bradycardia, htn, n/v, erectile dysfunction, loss of glycemic control

Atenolol inter

anticholinergics can decrease GI absorption, use w digoxin can cause AV block, additive effect w other antihypertensives

Atenolol NC/T

monitor bp and pulse, taper off, do NOT stop abruptly cause it can cause dysrhythmias (BBW), angina, MI. Monitor diabetes and change positions slowly

Digoxin class and MOA

cardiac glycoside, inhibits sodium-potassium pump and muscle cells have increased intracellular calcium concentration and increased efficiency of cardiac muscle fiber contractions. Acts of cardiac myocytes and the electrical conduction system

Digoxin TE

positive inotropic (increases strength of contractions), negative chronotropic (slows down time aka bpm), NOT A FIRST LINE MED

Digoxin con

2O or 3O heart block, ventricular dysrhythmias, acute MI, ctn with hypokalemia, hypothyroidism, renal disease, geriatrics

Digoxin SE

bradycardia, n/v, anorexia, life threatening (dysrhythmias, AV block, severe bradycardia), signs of toxicity (blurred vision, halo vision aka yellow, photophobia, changes in color perception, malaise, bradycardia)

Digoxin inter

diuretics, ACE, IV calcium, cardioactive drugs

Digoxin NC/T

monitor apical pulse before administering (hold if <60), assess for toxicity, narrow therapeutic range (<2.0), monitor K+ level and electrolytes and kidney function, antidote for digoxin immune FAB, frequent ECGs, take as prescribed, don’t discontinue or change brands, teach pt to take own pulse accurately, keep follow-up visits and lab test, report adverse effects

Milrinone class and MOA

phosphodiesterase 3 inhibitor, blocks enzyme in cardiac muscle that breaks down cAMP and results in increased calcium for greater cardiac contractility

Milrinone TE

positive inotropic (increases strength of contractions), vasodilation, only for SHORT TERM treatment of acute advanced heart failure

Milrinone con

severe heart valve disease and existing dysrhythmias, correct fluid and electrolyte imbalance before administering 

Milrinone SE

ventricular dysrhythmias (10%), hypotension, toxic (dose is limited to 48 hrs), headache, n/v

Milrinone NC/T

monitor ECG and vital signs, monitor fluid and electrolyte status, administered by IV ONLY (titrate based on response), report angina immediately, may have acetaminophen for headache