CAD:ACS Notes PDF

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Med Surg – Hcal 2

CAD/ACS

CAD and ACS CAD VS. ACS     

Coronary Artery Disease (CAD) is a blood vessel disorder caused by atherosclerosis CAD is the most common type of CV disease Other names – arteriosclerotic heart disease, CV heart disease, ischemic heart disease, coronary heart disease Usually takes a long time to develop so impt to focus on people at risk and start treatment early Acute Coronary Syndrome (ACS) is s/s of severe CAD and includes unstable angina (UA) and myocardial infarction (MI)

PATHOPHYSIOLOGY    

Progressive disease that takes years to develop, once you have symptoms it’s well-advanced that is why it’s so impt to identify those at risk and make early lifestyle changes Fatty streak → lipid-filled muscle cells, begins by age 15, reverse by decreasing LDLs Fibrous plaque – narrowing of the lumen, starts at age 30 Complicated lesion → most dangerous stage, plaque becomes unstable, ulcerates, ruptures; platelets accumulate causing a thrombus that enlarges (see also Fig 34-1)

COLLATERAL CIRCULATION     

Influenced by genetic predisposition to angiogenesis and the presence of chronic ischemia Is helpful No time for development of collateral circulation with rapid-onset CAD or coronary spasm leading to a big risk for MI When occlusions occur gradually this happens, actually makes an MI less harmful b/c there is still blood flow In an MI in a young person with no obvious disease they don’t have this compensation and often have a more significant MI

RISK FACTORS 

Non-Modifiable – Age – Gender  White males – Ethnicity  African Americans and Native Americans are at higher risk – Family history – Genetics

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Problems include familial hypercholerolemia (need to aggressively monitor and begin early tx of cholesterol), lots of other factors that we don’t fully understand Modifiable & Contributing – HTN (>140/90) or (>130/80) with DX / CKD – Tobacco use (1+ ppd)  Increases catecholamines, causes platelet adhesion, carbon monoxide affects oxygen transport – Diabetes → increases risk 2 – 4 times – Elevated Serum Lipids (keep LDL < 100 (carry cholesterol to arteries), HDL > 40 (carry lipids away from arteries)  High cholesterol (>200)  Fasting Triglyceride(>150) – Physical inactivity  Inactivity → exercise increases fibrinolytic activity, increases HDL, improves insulin resistance, may help develop collateral circulation – Obesity → risk increases as weight increases (apple is worse than pear-shaped) – Metabolic syndrome → insulin resistance with obesity, HTN, high lipids, and high BS – Homocysteine levels  Vitamin B Complex can help lower homocysteine levels – Psychological states  Depression, stress, anxiety, anger/hostility; Type A personality; increases catecholamines and blood sugar – Substance abuse  Produces coronary spasms (cocaine & meth) Always focus your teaching on modifiable risk factors, b/c the pt can actually control those Highest risk is among white, middle-aged men, but after age 65 risk is higher in women (kills 10 times more than breast cancer) Most important modifiable risk factors → HTN, diabetes, tobacco use 

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PHYSICAL ACTIVITY 

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Frequency → most days of the week Intensity → moderate (brisk walking, hiking, biking, swimming) Type → isotonic  Isotonic → moving (not static – holding one position) (isometric exercises involve prolonged holding for a period of time – ie. planks, squat holds – they increase BP and often lead you to hold your breath), be careful with heavy weight lifting as it causes a swift increase in heart rate and a quick drop – Time → 30 minutes – Adding resistance 2 days/week helps Focus teaching/interventions on the following slides Physical activity increases fibrinolytic activity (ie. Decreases clot risk), encourages development of collateral circulation Resistance training can decrease insulin resistance

NUTRITION 

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Fat intake – Decrease in saturated fat and cholesterol increase in complex cards and fiber – 30% of calories most coming from mono / poly unsaturated fats – Decrease red meats, eggs, whole milk products Reduce or eliminate alcohol and simple sugars Increase omega-3 fatty acids (ie. Tofu, fish, soybeans, flaxseed, walnut, canola)

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– Help prevent fat deposits in arteries Take EPA and DHA supplements Review Therapeutic Lifestyle Changes (TLC) Diet (Table 34-3. p. 737) – Low saturated fat, low cholesterol – Calories controlled based activity level – No absolute restrictions, no rules for coffee (if patient is on a cardiac diet with coffee restrictions, it is due to patient being prone to tachycardia dysthymias) – TLC → decreased saturated fat & cholesterol (decreased red meat, egg yolks, whole milk), increase in complex carbs (whole grains, fruits, veggies) and fiber, also should limit alcohol intake and simple sugars Really based on lowering lipid levels → less than 200 mg cholesterol/day and high fiber How do we get people to change? Focus on practical, specific changes, help them modify their favorite recipes, don’t just throw rules at them Examples → change to 1% milk, add fish to their diet, modify their recipes, pastries/baked goods are high in fat & cholesterol & sugar Can still have peanut butter, can still have coffee May need to limit salt (remember salt is in dairy products)

CHOLESTEROL LOWERING THERAPY  

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Complete lipid profile q 5 yrs (start age 20) – >200 is at risk and should be treated Diet therapy first – Restrict calories to decrease weight – Decrease dietary fat and cholesterol – Increase physical activity Reassess cholesterol levels after 6 weeks of diet therapy – If diet therapy doesn’t work and cholesterol is still high → then drug therapy is used Drugs are used concurrently with diet modification – Try diet changes before adding drug therapy Drugs are often needed for lifetime

CHOLESTEROL LOWERING DRUGS 

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Statins – Inhibit cholesterol synthesis in the liver – Take in the evening (b/c in the evening is when highest level of cholesterol is made) – Serious side effect is rhabdomyolysis, liver damage  Simvastatin, Atorvastatin, Rosuvastatin  Rhabdomyolysis S/S → muscle aches and pains, dark urine Niacin – Inhibits cholesterol synthesis – Many adverse effects (ie. Severe flushing, itching, GI probs, orthostatic hypotension)  Niacin, Nicotinic Acid – Niacin → commonly causes severe chest, neck, face flushing (lasts about 1½ hrs after taking); doesn’t mean they have to quit taking it, can take NSAIDs 30 minutes before to help with the symptoms  If no hives or wheezing is present with flushing = not an allergic reaction Fibric Acid Derivative – Won’t affect LDLs but is given to stop VLDLs  VLDLs specifically target the coronary arteries – May cause GI problems, interacts with many drugs (competes with liver P4 enzyme)  Gemfibrozil (Lopid), Fenofibrate ( TriCor)

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Bile Acid Sequestrants – Increase conversion of cholesterol to bile acids to get rid of cholesterol – Needs to be given 2 hrs. apart from other meds  Because if this is given with other meds, due to destroying cholesterol and ridding it with the body, the other medications can go with the cholesterol flush from the body  Cholestyramine (Questran), Colesevelam (Welchol)  Questran, Welchol → need to give 2 hrs apart from any other meds due to risk of interactions (ie. coumadin, thiazides, thyroid, beta blockers) Cholesterol Absorption Inhibitor – Inhibits absorption of dietary and biliary cholesterol – Often used with diet changes for primary hypercholesterolemia – Works really well when combined with statins  Ezetimibe (Zetia)

ANTIPLATELET THERAPY   

Most people with CAD should be on low-dose ASA (81 mg) – Not as effective for women until >age 65 – 81 mg of aspirin has the same antiplatelet effect as 325 mg of aspirin but less GI problems For high risk women (and/or men) intolerant of ASA use clopidogrel (Plavix) Beware of GI bleeding and hemorrhagic stroke symptoms – Make sure you know the s/s of GI bleeding and hemorrhagic stroke

GERONTOLOGIC CONSIDERATIONS   

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Although the incidence is high, risk reduction and CAD tx are worthwhile Aggressively treat HTN, hyperlipidemia, and stop smoking Planned physical activity: – Longer warm-ups – Longer period of low-level activity – Longer rest period between sessions – Avoid extremes of temperature This means we should still try to prevent and still treat even if a person is older Still helpful to stop smoking and treat other chronic conditions, still helpful to exercise

ANGINA  

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Also called angina pectoris (“strangling of the chest”) Temporary imbalance between oxygen supply and the heart’s demand – Temporary imbalance between the coronary’s ability to supply oxygen and the heart’s demand for oxygen, usu. caused by a stable atherosclerotic plaque, doesn’t cause permanent damage b/c ischemia time is so short Usu. caused by a stable, atherosclerotic plaque – To cause true ischemia typically has to be obstructed by 75% or more – Anything that increases O2 demand without the O2 supply and there is a plaque build up – angina can happen. Once person sits down and takes Nitro the heart relaxes and pain goes away Does not cause permanent damage – Doesn’t cause permanent damage b/c ischemia time is so short Can be stable or unstable Patho → myocardium becomes hypoxic w/in 10 seconds of occlusion (with total occlusion contractility will stop after several minutes) shifts from aerobic metabolism to anaerobic

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metabolism begins and lactic acid accumulates, lactic acid irritates myocardial nerves and sends a pain message (cause of chest pain), cardiac cells are viable for about 20 minutes when ischemic

PRECIPITATING FACTORS OF ANGINA        

Physical exertion Temperature extremes Strong emotions Eating a heavy meal Tobacco use Sexual activity Stimulants (ie. Cocaine, amphetamines) Circadian rhythm patterns (early am)

CHRONIC STABLE ANGINA 

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Chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity – Pressure, ache, constrictive, squeezing (not sharp or stabbing) – Pain does not change with position or breathing – May also have indigestion – Can have radiation of the pain Pain lasts 5-15 minutes – Greater than 15 minutes = unstable angina Usu. controlled with rest or meds to provide peak effects when angina usually occurs Occurs in a pattern that is familiar to the patient, Important to be able to recognize a change in the pattern that might suggest unstable angina and MI Pain level itself doesn’t matter Must be able to compare this with other types of chest pain to determine what’s bad (table in several more slides)

OTHER TYPES   

Silent ischemia → ischemia without symptoms (ie. Diabetics) – Ischemia that occurs in the absence of any subjective symptoms, more common in diabetics b/c of diabetic neuropathy affecting the nerves of the CV system, find it during monitoring Nocturnal angina → occurs only at night – Nocturnal only occurs at night but not necessarily when laying down or sleeping, decubitus only occurs when lying down and is relieved by standing or sitting Prinzmetal’s angina → often occurs at rest, seen with migraines and Raynaud’s, coronary spasm; need calcium channel blockers and/or nitrates – Variant angina that occurs at rest usu. in response to a major coronary artery spasm c/b increased intracellular calcium, rare and is usually seen by pts with a history of migraines and Raynaud’s phenomenom, may not have CAD, pain may resolve with moderate exercise,

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may get cyclic, short bursts of pain at a usual time each day; tx is calcium channel blockers and/or nitrates

DIAGNOSTIC TESTS 

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12-lead ECG – Compare with previous – Expect some mild ischemic changes CXR – Look for heart enlargement, calcifications, pulmonary problems Labs – Confirm CAD – Look for risk factors If known CAD:  Echo  Exercise stress test  Cardiac cath (maybe)

DRUG THERAPY 

Short-Acting Nitrates (1st line tx) – Should relieve pain in 3 minutes and lasts 30-60 minutes – Check BP, don’t give if 20 min – Can be atypical Sweating, ashen, clammy = poor CO Increased BP & HR (drops later) d/t release of catecholamines early in MI Crackles d/t left ventricular failure, can come and go for the first few days JVD, hepatic engorgement, edema d/t right ventricular failure Nausea/vomiting from pain Temp up to 100.4° = inflammatory process from myocardial cell death High glucose levels – Often will have increased blood glucose levels (from stress and release of glucose from the heart damage) Denial Distant heart sounds, S3/S4, loud holosystolic murmur – Holosystolic → throughout systole Dysrhythmias → sinus tachycardia with PVCs, T wave inversion, ST elevation or depression, abnormal Q waves Process takes several hours to occur and area of infarction can continue to extend Symptoms can be absent if patient has neuropathy (ie. diabetes), women and older patients have more vague symptoms The far right ECG is called “tombstoning” b/c it is shaped like a tombstone and it’s a bad sign (damage)

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HEALING PROCESS     

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Dead cardiac cells release enzymes Leukocytes infiltrate, thinning the cardiac wall Glucose and free fatty acids are released Can see the necrotic zone by ECG changes (ie. ST elevation, pathologic Q waves) 10-14 days after a weak scar develops, but the heart is very vulnerable – When patient is recovering from an MI, as a nurse be very careful as to what activity level your patient is at – warn them that they have to take it easy or else they could have deadly complications 6 weeks after they are healed, but the scarred area is less compliant Normal cells will hypertrophy and dilate (ventricular remodeling) which can lead to heart failure Dead cardiac cells release enzymes (these are the serum cardiac markers we test for) Within 24 hrs leukocytes infiltrate the area (blue/swollen heart) About the 4th day neutrophils and macrophages are removing necrotic tissue causing that part of the heart wall to thin (gray heart with yellow streaks) Serum glucose levels are high (b/c glucose and free fatty acids are released by the catecholamine response) – stress response Collagen matrix begins to form scar tissue At 10-14 days after MI new scar tissue is weak (making the heart vulnerable to increased stress) (start seeing granulation tissue) By 6 weeks scar tissue has replaced necrotic tissue and is considered healed (although it may be less compliant tissue leading to ventricular dysfunction or heart failure), the myocardium compensates at the beginning by hypertrophy and dilation (ventricular remodeling), this can lead to heart failure

DX STUDIES FOR ACS 

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Serial ECGs (every 2-4 hrs) – Change in QRS, ST segment, T wave – Distinguish between STEMI (pathologic Q wave) and NSTEMI or UA (incomplete occlusion without a pathologic Q wave) – Look at the pattern among the 12 leads to find the coronary artery involved – Ischemia causes ST depression, T wave inversion – Injury (still reversible) causes ST elevation – Infarction causes pathologic Q wave and T wave inversion (occurs w/in hrs, may persist for months) 12-lead ECG is the first thing that should be done, ECG tells where ischemia and necrosis are (by the leads showing changes) STEMI → complete occlusion (ST elevation, T wave inversion, Pathological Q wave) NSTEMI or UA → partial occlusion (no patho Q wave, ST depression, may have T wave inversion) ST elevation is the most important change to watch for, if cardiac markers are also elevated then it is a STEMI and there is an infarct Pathologic Q wave is deep and wide (oftentimes a permanent change, ST depression and T wave inversion improve in hours to days) Remember the picture in symptom about the zone of ischemia and infarction? ECG may initially look normal and then change, this is why we do serial 12-lead ECGs every 2-4 hrs

DX STUDIES FOR ACS

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DX STUDIES FOR ACS    

LAD → Anterior portion of Heart – Anterior MI RCA → Inferior Portion of Heart – Inferior MI – Think here if patient has bradycardia Circumflex → Posterior, Lateral Portion of Heart – Posterior / Lateral MI Can have combination – Anterior Lateral MI = MI involving LAD & Circumflex Arteries

DX STUDIES 

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Serum cardiac markers (serially) – Cardiac Specific Troponin T (cTnT) & Cardiac Specific Troponin I (cTnI)  Initial: 4-6 hrs  Peak: 10-24 hrs  Baseline: 10-14 days  Troponin and CK-MB rise within 4-6 hours after MI, troponin peaks at 10-24 hrs, takes 2 weeks to normalize and CK-MB peaks in 18 hrs, normal w/in 24-36 hrs – CK-MB  Initial: 6 hrs  Peak: 18 hrs  Baseline: 10-14 days – Myoglobin  Initial: 2 hrs  Peak: 3-15 hrs  Released earliest but is non-specific  Myoglobin is rapidly excreted by the kidneys → rises within 2 hrs, peaks in 3-15 hrs, normal within 24 hrs ECG and cardiac markers are non-diagnostic, exercise or pharmacologic stress testing, echo, stress echo – Remember stress tests → looking for ECG changes when there is ischemia, can use drugs (ie. dobutamine, adenosine) if pt can’t tolerate exercise May even do coronary angiography

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Coronary angiography → shows extent of the disease so you know how to treat it and is the only way to confirm Prinzmetal’s angina, while they are in there they can do an intervention (PCI – ie. stents, balloon angioplasty, etc.) Indicates cardiac damage and cell death –

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TREATMENT             

Oxygen (2-4 L/min by NC), position upright FIRST! 12-lead ECG and continuous monitoring Chewable aspirin THIRD! Prevents further platelet aggregation SL nitroglycerin SECOND! Morphine IV if pain not relieved by NTG (given if nitro doesn’t work) Treat dysrhythmias VS with pulse ox frequently Bedrest for 12-24 hours NPO except sips of water until stable Goal is to salvage as much myocardial muscle as possible so need rapid diagnosis MONA = Morphine, Oxygen, Nitrates, Aspirin Pain management increases oxygen supply, decreases oxygen demand, decreases anxiety Why do we give Nitro first instead of going straight to morphine? Want to see if it is angina instead of MI

MI MEDICATIONS 

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Initially: O2 is given FIRST!! – IV Nitroglycerin (Tridil) – Morphine – Dual antiplatelet therapy  Aspirin  Clopidogrel (Plavix) – LMWH or IV heparin Within 24 hrs: – Oral beta-adrenergic blockers (if no contraindications) – ACE inhibitors (for some) – Antidysrhythmics (only if life threatening) – Lipid lowering drugs – Stool softener

TREATMENT 

If UA or NSTEMI without cardiac markers: – Aspirin – Heparin – Integrillin (antiplatelet) – Coronary angiogram with PTCA once stabilized and angina controlled

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If STEMI or NSTEMI with cardiac markers: – Reperfusion therapy (ie. Emergent PTCA, fibrinolytics, coronary surgical revascularization)

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA)      
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