Lewis's Medical-Surgical Nursing: Medsurge2 ch 33 Flashcards

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What is CAD

A blood vessel disorder caused by atherosclerosis


What is the most common type of CV disease



What are other names of CAD

Atherosclerotic heart disease

CV heart disease

Ischemic heart disease

Coronary heart disease


What is Acute Coronary Syndrome (ACS)

more serious manifestation of CAD such as unstable angina and myocardial infarction


What are the 2 leading contributing factors to CAD




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


Inflammatory mediators



Low density lipoproteins (LDL)



What happens within 10 seconds of your myocardial tissue being deprived of oxygen?

Shifts from aerobic to anaerobic metabolism to get more energy causing lactic acid to build up


Lactic acid

Chemical produced in body from being oxygen deprived

-irritating to nerves and heart causing that crushing chest pain


What will prevent actual cell death

Restoring oxygenated blood back to myocardial tissue within 20 minutes


Oxygen supply vs oxygen demand

Supplying sufficient oxygenated blood

Can’t meet the oxygen demand so the tissue shifts from aerobic metabolism to anaerobic metabolism


Blood clot

Ultimately causes a heart attack/ obstruction


What increases platelet aggregation in CAD?

Inflammatory mediators and the inflammatory response stick together eventually creating a blood clot



Reduces severity of MI by reducing platelet aggregation in blood


In most cases young people have the advantage to

Recover quicker because they have less co-morbidities


When it comes to MI/ heart attacks; young people have

Disadvantage because they are not common in young people and they don’t have time to develop collateral circulation

-usually caused by drugs in the young


Collateral Circulation

Compensation for blocked arteries by creating new pathways to maintain blood flow

-develops overtime in people with years of CAD


What are Modifiable risk factors

Things we can do to help decrease our risk of a heart attack


Modifiable risk factors includes:

Diet, exercise, weight loss, smoking cessation, reduce alcohol intake


Diet education

Low cholesterol, low triglycerides

Limit sugar intake in diabetics


Why is Weight loss important in CAD?

Obesity contributes to hypertension and diabetes; the two leading contributing factors of a stroke


Why is Exercise beneficial in CAD patients

Physical activity increases fibrinolytic activity (Decreases clot risk)

-Encourages development of collateral circulation


How does Smoking / nicotine affect your heart?

Strains your heart by causing it to increase/ putting unnecessary stress on it

-also breathing in poison


How does Alcohol contribute to CAD

Contains a lot of sugar and can contribute to obesity and hypertension


At age 20

It is recommended to get a complete lipid profile Q 5 years


Cholesterol lowering therapy:

first step

Diet therapy first

-restrict calories to decrease weight

-decrease dietary fat and cholesterol

-increase physical activity


Cholesterol lowering therapy:

second step

Reassess cholesterol levels after 6 weeks of diet therapy


What organ produces Cholesterol

The liver


Cholesterol lowering therapy:
possible 3rd step if the first two aren’t enough

Cholesterol lowering drugs

- can be on these for life


Cholesterol lowering drugs

Statins, Niacin’s, Fibric Acid derivatives

-all commonly cause G.I problems



Simvastatin, Atorvastatin,Rosuvastatin

Inhibit cholesterol synthesis in the liver

-Take in the evening (most cholesterol is synthesized at night)

-serious side effects: rhabdomyolysis, liver damage

Rhabdomyolysis s/s – muscle aches and pains, dark urine



Niacin, Nicotinic Acid

Inhibits cholesterol synthesis in the liver

-Adverse effects: severe flushing, itching, G.I problems, orthostatic hypotension

-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


Fibric acid derivative

Gemfibrozil (Lopid), Fenofibrate (TriCor)

Won’t affect LDL’s; affects VLDL’s (second type of bad fatty acid that specifically targets coronary arteries)

May cause G.I problems; interacts with many drugs

-causes other meds to reach toxicity blood levels

-always get med list!


Bile Acid Sequestrants

Cholestyramine (Questran), Colesevelam (Welchol)

Increase conversion of cholesterol to bile acids by binding to bad cholesterol and bringing it at a quicker rate to the liver

-needs to be given 2 hrs apart from other meds because it can cause it to be sub-therapeutic



Creates Cholesterol and also destroys cholesterol by turning the cholesterol into bile acids


Cholesterol Absorption Inhibitor

Ezetimibe (Zetia)

Inhibits absorption of dietary and biliary cholesterol

-often used with diet changes for primary hypercholesterolemia

-works really well when combined w/ statins


Platelet aggregation inhibitor therapy

Most people w/ CAD should be on low-dose Aspirin (81mg)

-beware of G.I bleeding and hemorrhagic stroke symptoms (abdominal pain, black tarry stools, blood tinged stool)


Clopidogrel (Plavix)

Anti platelet aggregating med

-For high risk men and women or intolerant to aspirin

- high risk for bleeding! Watch platelets and h&h


Gerontologic considerations

Although incidence is high; risk reduction and CAD tx are worthwhile


CAD tx includes

Aggressively tx hypertension,hyperlipidemia, and smoking cessation


Older adults planned physical activity should include

Longer warm ups

longer period of low-level activity

longer rest period between sessions

avoid extreme temperatures


The faster your hearts going..

The more you’re in systole (contracting); and pushing blood out of the heart


During diastole

The heart is the only organ being fed blood (ventricles relax and fill with blood)



“angina pectoris”

Chest pain caused by temporary imbalance between oxygen supply and the heart’s demand; usually caused by a stable atherosclerotic plaque

-“compression, constriction, squeezing, pressure” sensation

-constant pain regardless of position



Sharp stabbing pain in the chest caused by inflammation of the lining of the heart (pericardium sac)

-pain relieved by leaning forward and breathing out

-pain intensifies when you’re breathing in


Pathology of Angina

myocardium becomes hypoxic w/in 10 seconds of occlusion (with total occlusion contractility will stop after several minutes), anaerobic 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

-lactic acid can spread which is why there is radiating pain to your left shoulder or radiating up and down your left arm, even up to your jaw


Unstable Angina

New chest pain, pain that occurs at rest, pain that has worsening pattern or uncontrolled chest pain that does not resolve with meds and stopping the trigger is indicative of an MI

-women have prodromal symptoms


Stable angina

Controlled chest pain that usually goes away once the trigger is stopped and some niacin/ nitroglyceride is administered

-usually doesn’t damage heart


Common causes 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)


25-30% cardiac output is used

In your G.I system to help digest food

- can go up to 35% after a heavy meal


CAD diet education

Reduce fats, consume a healthier diet, and smaller portions


Chronic stable angina

Chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity(Pressure, ache, constrictive, squeezing)

-Pain does not change with position or breathing

-May also have indigestion

-Can have radiation of the pain

-Pain lasts 5-15 minutes

-Usually controlled with rest or meds to provide peak effects when angina usually occurs


Prinzmetals angina

Chest pain due to coronary artery spasms; may get cyclic, short bursts of pain at a usual time each day

-tend to see it more w/ people who have a history of migraines, Raynaud’s disease, pt.’s with higher levels of calcium in their blood

-tx with calcium channel blockers or nitrates

-pain may resolve with moderate exercise


Silent Ischemia

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


Decubitus angina

only occurs when lying down and is relieved by standing or sitting


Why are 12 lead ecg’s used?

Compares with previous

expect some mild ischemic changes

gives us an estimate of where the heart is being affected


Purpose of a Chest xray

Looks for enlarged heart and pulmonary problems


Purpose of Labs

Confirms CAD

looks for risk factors

(lipid panel, blood glucose, hemoglobin a1c)


Diagnostic: Echocardiogram

Sees how well our heart is pumping / ejection fraction


Diagnostic: exercise stress test

Increases physical demand to increase heart rate while simultaneously monitoring ecg


Short acting Nitrates

First line of therapy

dilates peripheral blood vessels and coronary arteries/collateral vessels

IV Nitril – reduces anginal pain, improves coronary blood flow/oxygen supply, decreases preload and afterload; titrated to control chest pain

*must monitor BP*


Things to know about short acting nitrates

Should relieve pain in 3 minutes and lasts 30-60 minutes
Check BP, don’t give if <100

1 tab SL or 1 spray under tongue (allow to dissolve) (may cause tingling, increased HR, headache, dizziness, flushing)

If sx unchanged after 5 minutes, call EMS

If sx improved after 5 minutes continue every 5 minutes for a max of 3 doses until completely resolved or call EMS

Never give if pt has taken Viagra=vasodilatador

Monitor for orthostatic hypotension

Store NTG away from light and heat

Replace NTG every 6 months

Can take 5-10 minutes before provoking activities

Watch for changes in the usual pain pattern


Long acting nitrates

Isordil (Isosorbide dinitrate), Imdur (isosorbide mononitrate)

used to reduce incidence of angina attacks

causes headache & orthostatic hypotension

Can take SL Nitro for breakthrough pain if using long-acting nitrates


Beta blockers -lol

Decreases myocardial oxygen demand (reduces BP, HR, contractility), decreases risk of reinfarction and occurrence of HF; not used if at risk for cardiogenic shock

*assess HR and BP before giving*

Preferred drug for chronic stable angina and following an MI; Has cardio protection by covering the beta receptor when you’re having a heart attack

many side effects (low HR, low BP, wheezing)


ACE inhibitors -pril

prevents ventricular remodeling, prevents/slows the progression of HF

Can cause low BP, change in potassium levels, angioedema, and a nonproductive cough



Calcium channel blockers -pine

also Verapamil, Diltiazem

Used when beta blockers are contraindicated or don’t work; cause decrease BP and HR by increasing vasodilation

used for Prinzmetal’s angina (tend to have higher level of calcium)

Use with angina but not after MI

*Can cause digoxin toxicity


Globular infiltration rate = GFR

how much blood we filter per minute

normal filtration rate= 90 - 120 ml/ min


Kidneys release_____ to trigger the_____in order to create _____ which is converted into ___ through _____

Release renin to trigger the RAAS pathway in order to create angiotensin 1 which is converted into angiotensin 2 through Angiotensin converting enzymes


Angiotensin 2


causes the release of aldosterone



Causes us to reabsorb sodium and water and get rid of potassium


Left ventricular remodeling

Left ventricle starts becoming thicker due to overexertion


Acute Coronary Syndrome (ACS)

Associated with deterioration of a plaque causing partial occlusion (UA, NSTEMI) or total occlusion (STEMI) by thrombus

-Develops when ischemia is prolonged, usually a plaque ruptures causing platelets to clump and clots to form, vasoconstriction occurs; all of this contributes to narrowing of the coronary arteries and prolonged ischemia


Classifications of an NSTEMI / UA

-no pathological Q wave

-ST segment depression

-May or May not have an inverted T wave

-troponin let’s us know whether it’s an actual MI or not


Classifications of a STEMI

ST elevated MI = total occlusion (100% blockage)

-Will have a pathological Q wave (drops way down and becomes wider)

-will have ST segment elevation (looks like a tombstone)

-may or may not have an inverted T-wave



Cardiac enzyme that proves there is cell death

-used to confirm an MI because it increases quicker than CK

-rises within 4-6 hours after MI, troponin peaks at 10-24 hrs, takes 2 weeks to normalize


Prodromal symptoms

Basically other uncommon symptoms
-Fatigue, dyspnea, indigestion, anxiety


Acute myocardial Infarction

heart attack

Sustained ischemia (>20 min) causing irreversible myocardial cell death (4-6 hrs to necrose entire thickness of the heart)

-Most due to thrombus

-Most involve some portion of the left ventricle

-25% of MI’s are anterior wall with obstruction of the LAD and left ventricular dysfunction

-Usually described based on location of the damage (ie. Anterior, inferior, lateral, etc.), this damage correlates to what artery was involved


Signs & symptoms of an MI

Severe, immobilizing chest pain not relieved by rest, position change, nitrates or antacids(More common in early am, Lasts > 20 min, Can be atypical)

-Sweating, ashen, clammy – poor CO

-Increased BP, HR 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 and vomiting from pain (build up of lactic acid) or acid reflux

-Temp. elevation (100.4)– inflammatory process from myocardial cell death

-Often will have increased blood glucose levels (from stress and release of glucose from the heart damage)

-Distant heart sounds, S3/S4, loud holosystolic murmur


Cardiogenic shock

you’re not using your body effectively because there’s something going on with the pumping mechanism of your heart


Blood flow through the heart

Right atrium sends blood to the right ventricle to pump blood into the lungs to become oxygenated; delivering it to the Left atrium, sending blood to the left ventricle which pumps oxygenated blood to your body


Healing process after an MI

Within 24 hrs leukocytes infiltrate the area (blue/swollen heart)

Dead cardiac cells release enzymes (these are the serum cardiac markers we test for)

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)

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


Serial ECG’s

ECG’s every 2-4 hours

-12-lead ECG is the first thing that should be done, ECG tells where ischemia and necrosis are (by the leads showing changes)


Coronary angiography

shows extent of the disease so you know how to treat it; while they are in there they can do an intervention (PCI – ie. stents, balloon angioplasty, etc

-is the only way to confirm Prinzmetal’s angina



Stored iron in your muscle cells; least specific when it comes to cardiac

-rapidly excreted by the kidneys

–rises within 2 hrs, peaks in 3-15 hrs, normal within 24 hrs


Creatinine Kinase (CK-MB)

Cardiac enzyme released whenever there is muscle cell death

-MB is the subcategory of type of tissue

-CK-MB increases in 6hrs, peaks in 18 hrs, normal w/in 24-36 hrs


Treatment with NSTEMI

Goal is to salvage as much myocardial muscle as possible so need rapid diagnosis; MONA – Morphine, Oxygen, Nitrates, Aspirin

-vitals w/ cont. pulse ox

-12 lead ecg w/ continuous monitoring
-Bedrest 12-24 hours

-NPO w/ sips of h2o until stable

platelet aggregation inhibitors (aspirin, clopidogrel [plavix], heparin, LMWH)

Pain management increases oxygen supply, decreases oxygen demand, decreases anxiety



For chest pain unrelieved by NTG, vasodilates (lowers myocardial oxygen consumption, decreases contractility, decreases BP and HR), reduces anxiety

*must monitor for resp. depression and low BP*


Percutaneous Transluminal Coronary Angioplasty (PTCA)

Heart cath.

-1st line tx w/ confirmed MI; goal is to open the artery w/in 90 min
-Local anesthesia, walking w/in 24 hrs, home in 1-3 days, work in 1 wk

-Requires antiplatelet drugs; IV drugs (Integrillin) or sometimes heparin during and 12 hrs after the procedure; Oral antiplatelet drugs (ASA, Plavix) for 6-9 months


Percutaneous Transluminal Coronary Angioplasty (PTCA) - Post procedure education

Post procedure - watch for chest pain, bleeding, abrupt closure (will have same symptoms as they admitted for), vascular injury, AMI, stent embolization, coronary spasm, dysrhythmias

Nursing care after - watch for clotting (CMST of affected leg q 15 min), watch for bleeding (look at the sheets, never remove pressure dressing, watch VS q 15 min)

check insertion site! Check for hematomas, shadowing, check pulse, temperature,color etc…


Muffled heart sounds

Indicative of a cardiac tamponade



Have massive bruising


Fibrinolytic therapy

Done if there is no cath lab; Only given IV!

-goal is stop infarction process by dissolving the thrombus & reperfusing myocardium

-Give ASAP (ideally w/in 1st hr after symptoms; must be within 6 hrs – goal is w/in 30 minutes of arrival)

-Absolute contraindications – active internal bleeding or bleeding problems, known hx of cerebral aneurysm or AV malformation, known intracranial neoplasm, previous cerebral hemorrhage, recent (within past 3 months) ischemic stroke, significant head or facial trauma in past 3 months, suspected aortic dissection

-will usually be on aspirin and IV heparin drip or SC Lovenox to maintain patency of the coronary artery


Fibrinolytics nursing care

-baseline lab values

- start 2-3 I.V lines

-Get all invasive procedures done if possible
-Give in one IV bolus or over 30-90 minutes

-Closely monitor (rhythms, VS, pulse ox, heart/lung/neuro/bleeding assessments)


How do you know when reperfusion occurs?

-Return of ST segment to baseline

-Abrupt cessation of chest pain

-Early, rapid rise of cardiac enzymes w/in 3 hrs, peaking at 12 hrs; CK prematurely rises (within minutes, peaking in hours) b/c the blood reperfuses the ischemic tissue “washing out” the CK

-May have sudden onset of reperfusion dysrrhythmias; Reperfusion arrythmias are usu. self-limiting and do not require aggressive treatment (ie. Non-sustained [brief] Vtach, PVCs, sinus bradycardia), happens when the ischemic myocardium is reperfused


Heart cath serves as a…

Diagnostic because it confirms and locates the blockage


Coronary artery bypass graft (CABG)

Done on patients who cannot have a stent placed or not going to benefit from it

-Have left main coronary artery, 3-vessel disease, are not candidates for PTCA, failed PTCA with ongoing chest pain


What are the arteries/ veins used for the CABG?

internal mammary artery (IMA) - 10 year patency rate [no additional interventions]

saphenous vein [need to monitor leg incision]

radial artery -tends to spasm because it has more smooth muscle [need to do CMST- circulation, motion, sensation ,temperature]


MIDCAB – minimally invasive direct coronary artery bypass

no sternotomy, no CPD, several small incisions by the ribs, heart stopped using drugs


OPCAB – off pump coronary artery bypass

only done if very sick


Nursing care after CABG

-In ICU for 24-36 hrs with PA catheter, arterial line, chest tubes, continuous ECG monitoring, ETT, epicardial pacing wires, urinary catheter, NGT

-Usu. extubated w/in 6 hrs and to step-down in 24 hrs

-Postop dysrthymias (esp. atrial) in first 3 days


Removed artery/ vein nursing cares

IMA – lots of pain, chest tubes; no interventions

Radial graft – CMST, open and close hand several times a day to promote circulation

Saphenous – edema is common, don’t cross legs, wear TED hose, elevate


Post op complications from Coronary bypass

    • Systemic inflammatory response syndrome (SIRS)
    • Fluid & electrolyte imbalance
    • Hypothermia
    • Bleeding
    • postop dysrythmias (especially atrial) in 3 days

Sudden Cardiac Death

-Caused by acute ventricular dysrhythmias, sometimes a ventricular obstruction or extreme bradycardia (usu. not an AMI)

-May or may not have known CAD
-Death usu. occurs w/in 1 hr of symptoms, most have no warning s/s
-If they survive, they are at high risk for another event


Surviving Sudden cardiac death tx

-Diagnostic workup for MI
-Cardiac cath (may need PCI or CABG)
-24 hr Holter monitor, exercise stress test, EPS (electrophysiologic lab)
-ICD to prevent a recurrence
-May be given lidocaine, procainamide or sotalol
-Help them with the psychological implications