NURS-300 Exam 1: Lecture 9 (Coronary Artery Disease & Acute Coronary Artery Syndrome)

CAD Health Promotion Behaviors

1.) Physical fitness: → FITT formula: 30 minutes >5 days/week. → Regular physical activity contributes to: ⤷ Weight reduction. ⤷ Reduction of >10% in systolic BP can be seen with weight reductions of 20 pounds. ⤷ In some men more than women, an increase in HDL cholesterol. 2.) Cholesterol-lowering drug therapy: → Drugs that restrict lipoprotein production: Statins, niacin. → Drugs that increase lipoprotein removal: Bile acid sequestrants. → Drugs that decrease cholesterol absorption: Ezetimibe (Zetia). 3.) Antiplatelet therapy: → ASA. → Clopidogrel (Plavix).

Sudden Cardiac Death Etiology and Pathophysiology

1.) Primary risk factors: → Left ventricular dysfunction (EF 30%). → Ventricular dysrhythmias following MI. 2.) Other risk factors: → Male gender (especially African American men). → Family history of premature atherosclerosis. → Tobacco use. → Diabetes mellitus. → Hypercholesterolemia. → Hypertension. → Cardiomyopathy.

Clinical Manifestations of ACS Myocardial Infarction (MI)

1.) Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis). 2.) Necrosis of entire thickness of myocardium takes 4 to 6 hours. → This is important because there are certain clot busting drugs that you can give patients, but you have to make sure you are within that 4-6 hour window. → If you give it outside of this window you are going to be opening up the blood vessel to dead tissue. 3.) The degree of altered function depends on the area of the heart involved and the size of the infarct. 4.) Contractile function of the heart is disrupted in areas of myocardial necrosis. → This is where some of the lethal rhythms come in. 5.) Most MIs involve the left ventricle (LV).

Clinical Manifestations of CAD

1.) Shortness of breath. 2.) Arrhythmias (if certain parts of the heart are damaged). 3.) Heart failure. 4.) Angina pectoris. → Reversible (temporary) myocardial ischemia = angina (chest pain). ⤷ O2 demand > O2 supply. ⤷ Relieved by rest and/or nitroglycerine (opens up blood vessels). 5.) Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis. → For ischemia to occur, the artery is usually 75% or more stenosed.

Chronic Stable Angina Other Variants

1.) Silent ischemia: → Up to 80% of patients with myocardial ischemia are asymptomatic. → Associated with diabetes mellitus and hypertension. → Confirmed by ECG changes. 2.) Nocturnal angina: → Occurs only at night but not necessarily during sleep. 3.) Angina decubitus: → Chest pain that occurs only while lying down. → Relieved by standing or sitting.

Atherosclerosis Causes

1.) The exact cause of atherosclerosis isn't known. However, studies show that atherosclerosis is a slow, complex disease that may start in childhood. It develops faster as you age. 2.) Atherosclerosis may start when certain factors damage the inner layers of the arteries causing injury and inflammation. → Overtime this cycle of injury, inflammation, and repair leads to the buildup of plaques which narrow the arteries. 3.) These factors include: → Smoking. → High amounts of certain fats and cholesterol in the blood. → High blood pressure. → High amounts of sugar in the blood due to insulin resistance or diabetes.

Sudden Cardiac Death (SCD)

1.) Unexpected death from cardiac causes. → Most deaths occur outside of hospital. → CAD accounts for about 80% of all SCDs. 2.) Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow. 3.) Death usually within 1 hour of onset of acute symptoms (e.g., angina, palpitations). 4.) Most SCDs caused by ventricular dysrhythmias (e.g., ventricular tachycardia).

Clinical Manifestations of ACS Unstable Angina

1.) Unstable angina: Different characteristics from chronic stable angina. → New in onset. → Occurs at rest (no precipitating factor). → Has a worsening pattern. 2.) UA is unpredictable and represents a medical emergency. → If you do not get them help the patient may quickly deteriorate and die.

Risk Factors for Developing CAD (continued)

Risk factors can be categorized as: Modifiable risk factors. 1.) Elevated serum lipids. → We can get them on cholesterol lowering drugs, get them with social work (make sure they can pay for their medications). 2.) Hypertension. 3.) Tobacco use. 4.) Physical inactivity. 5.) Obesity. 6.) Heavy alcohol use. 7.) Diabetes. 8.) Metabolic syndrome (aka insulin resistance) → Tied to abdominal obesity, high Triglyceride levels, low HDL cholesterol levels, high blood pressure and fasting blood sugar. 9.) Psychological states. 10.) High Homocysteine level (amino acid in the blood).

Risk Factors for Developing CAD

Risk factors can be categorized as: Non-modifiable risk factors. 1.) Age & Gender. → In men, the risk increases after age 45. → In women, the risk increases after age 55. 2.) High levels of a protein called C-reactive protein (CRP) in the blood (not understood well because it is not a specific for marker for arterial wall inflammation). 3.) Ethnicity. 4.) Family history. 5.) Genetic predisposition.

Serum Cardiac Markers After MI

These tests are testing how fresh the MI is. There are different markers that peak at different times to help you know when this heart attack occurred.

Placement of a Coronary Artery Stent

A lot of times stents fail! The artery will put pressure on the stents sometimes causing them to collapse (can add to more narrowing or problems in the area).

ACS/MI Nursing Management (continued)

1.) Perform 12 lead ECG immediately with any new pain or change in level or character of pain. 2.) Monitor respirations, breath sounds, and I/O to detect early signs of heart failure. → Will let you know how much of the heart is involved and whether dysfunction is being developed overtime due to weakening of the heart tissue. → I/O might show you that the heart is not pumping adequate blood flow to target organs like the kidneys. 3.) Monitor O2 saturations and administer O2 via nasal cannula 2-4 liters to increase oxygenation to the heart. 4.) Provide rest to decrease O2 demands of the heart.

Confusing Terminology

1.) Arteriosclerosis: → Is a general term describing any hardening (and loss of elasticity) of medium or large arteries. 2.) Atherosclerosis: → Is a hardening of an artery specifically due to an atheromatous plaque. → It is the most common form of arteriosclerosis and characterized by the thickening of the intima with plaques that contain lipid-laden macrophages ("foam"). → The plaques contain free lipid (cholesterol) and are prone to calcification and ulceration. ⤷ When these plaques ulcerate it causes the vessels to bleed and the blood can form a clot which can occlude a vessel (leads to heart attacks and strokes). 3.) Arteriolosclerois: → Is any hardening (and loss of elasticity) of arterioles (small arteries). → It is often due to hypertension and diabetes mellitus.

ACS/MI Nursing Management

1.) Assess Pain frequently (pain usually first presenting sign of MI). → If pain is not being relieved then the ischemia is not going away! 2.) Assess hemodynamic status: → BP, LOC (if the heart is not pumping enough to the brain it will cause alertness issues), HR, Skin color, and temperature (every 5 minutes during episodic pain every 15 minutes post pain). 3.) Monitor continuous EEG to detect Dysrthythmias.

Myocardial Infarction Healing Process (continued)

1.) By 6 weeks after MI, scar tissue has replaced necrotic tissue. → Area is said to be healed, but less compliant (never the same!). 2.) Ventricular remodeling. → In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate.

Complications of Myocardial Infarction (continued)

1.) Cardiogenic shock: → Occurs when inadequate oxygen and nutrients are supplied to the tissues throughout your body because of severe LV failure. → Requires aggressive management. 2.) Papillary muscle dysfunction: → Causes mitral valve regurgitation (if the tissue around the valve is damaged it might not function properly). → Condition aggravates an already compromised LV. 3.) Ventricular aneurysm: → Results when the infarcted myocardial wall becomes thinned and bulges out during contraction (could burst and cause immediate death). → Then, a lot of the blood is not being pumped throughout the rest of the body. The out pouching could cause pooling of blood and clots to form leading to other problems throughout the body once it gets ejected (brain, liver, kidney, etc./could lead to a stroke).

Clinical Manifestations of ACS MI (continued again)

1.) Cardiovascular: → Initially, ↑HR (trying to pump blood to places that are lacking) and BP, then ↓BP (secondary to ↓in CO). → Crackles (blood backs up into the pulmonary system). → Jugular venous distention. → Abnormal heart sounds. ⤷ S3 or S4. ⤷ New murmur. 2.) Nausea and vomiting: → Can result from reflex stimulation of the vomiting center by the severe pain. 3.) Fever: → Systemic manifestation of the inflammatory process caused by cell death.

Diagnostic Studies Unstable Angina & MI

1.) Detailed health history and physical. → Know when the pain is getting worse going from chronic stable angina to a MI. 2.) 12-lead ECG: Changes in QRS complex, ST segment elevation, and T wave inversion can rule out or confirm UA or MI. 3.) Serum cardiac markers: → See next slide. 4.) Coronary angiography. → See where blockages are and see if a stent can go in to fix the blockage. 5.) Others: Exercise stress testing, echocardiogram.

Acute Coronary Syndrome Etiology and Pathophysiology

1.) Deterioration of a once stable plaque ▻ rupture ▻ platelet aggregation thrombus ▻ 2.) Result: → Partial occlusion of coronary artery: UA or NSTEMI → Total occlusion of coronary artery: STEMI

Complications of Myocardial Infarction

1.) Dysrhythmias: → Most common complication. → Present in 80% of MI patients. → Most common cause of death in the pre-hospital period. → Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock. 2.) Heart failure: → A complication that occurs when the pumping power of the heart has diminished.

Clinical Manifestations of ACS MI (continued)

1.) Fear and anxiety (impending doom). 2.) Dyspnea. 3.) Sympathetic nervous system stimulation results in: → Release of glycogen. → Diaphoresis (pale and clammy). → Vasoconstriction of peripheral blood vessels. → Skin: Ashen, clammy, and/or cool to touch.

ACS/MI Medication therapy

1.) Fibrinolytic therapy (clot busting drugs). → Activase, t-PA (tissue plasminogen activator, or steptokinase). → Dissolve clots. → Monitor for bleeding plus signs of CVA. → Only useful if given within 4-6 hours. 2.) IV nitroglycerin (vasodialator). 3.) Anticoagulants (prevent additional clot formation). → Ex. Heparin. 4.) Morphine sulfate (pain). 5.) β-adrenergic blockers. 6.) Angiotensin-converting enzyme inhibitors. 7.) Antidysrhythmia drugs. 8.) Cholesterol-lowering drugs. 9.) Stool softeners. → Exacerbate new scar tissue that is starting to develop.

Stable Angina Diagnostic Studies

1.) Health history/physical examination. 2.) Laboratory studies. 3.) 12-lead ECG (look for rhythm changes or ST elevations). 4.) Chest x-ray. 5.) Echocardiogram. 6.) Exercise stress test. 7.) Cardiac catheterization (see blockages/extend of blockages). → Diagnostic. → Coronary revascularization: Percutaneous coronary intervention. ⤷ Balloon angioplasty. ⤷ Stent.

Types of Angina Chronic Stable Angina

1.) Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms. 2.) Pain usually lasts 3 to 5 minutes: → Subsides when the precipitating factor is relieved (exercise, exertion, straining on the toilet, etc.). → Pain at rest is unusual. → ECG reveals ST segment depression.

ACS/MI Nursing Management (continued again)

1.) Keep patient NPO (because they may need to get them into a procedure) or progress to liquid diet as ordered, maintain IV access. 2.) Provide calm environment to decrease stress, fear, and anxiety. 3.) Report significant changes immediately to ensure rapid changes. 4.) Maintain bedrest (with commode) for 24-36 hours and gradually increase activity as ordered while closely monitoring ECG, pain (especially any new pain). 5.) Progress diet from liquid to low sodium, low fat as ordered. → Get them a stool softener because you do not want them to strain. Try to lower oxygen necessity of the body!

Types of Angina Prinzmetal's Angina

1.) Occurs at rest usually in response to spasm of major coronary artery. → It can exhibit the same signs as chronic stable angina exhibit. 2.) Seen in patients with a history of migraine headaches and Raynaud's phenomenon. 3.) Spasm may occur in the absence of CAD. → When spasm occurs. ⤷ Chest pain. ⤷ Marked, transient ST segment elevation. → May occur during REM sleep. → May be relieved by moderate exercise (sometimes not always).

Atherosclerosis Pathway

1.) When damage occurs, your body starts a healing process sending in a team of inflammatory cells including white blood cells called monocytes. 2.) These monocytes migrate into the artery wall where they turn into macrophages and gobble up LDL cholesterol. 3.) These macrophages now stuffed with cholesterol form fatty streaks in the artery wall (really small to start with). 4.) Over decades more cholesterol, connective and elastic tissue, calcium, and cell debris accumulate and turn the fatty streak into a plaque (thicker). → The artery loses its elasticity and starts to narrow. 5.) As the artery tries to heal itself, smooth muscle cells migrate in to cover the plaque forming a fibrous cap. 6.) Macrophages kill smooth muscle cells and release enzymes that break down the fibrous cap. → This causes a weakening of the artery. 7.) The cap ruptures (something causes this; ex. hypertension) and cells called platelets clump together to form blood clots where the ruptures are. 8.) This narrows the arteries more and worsens angina (chest pain) or causes a heart attack. → This can totally occlude the vessel or only kinda do so.

Acute Coronary Syndrome

1.) When ischemia is prolonged (>3-5 minutes) and not immediately reversible, acute coronary syndrome (ACS) develops. → If you do not do anything about it they can have long term damage to their coronary tissue. 2.) ACS encompasses: → Unstable angina (UA). → Non-ST-segment-elevation myocardial infarction (NSTEMI). → ST-segment-elevation (STEMI).

Myocardial Infarction Healing Process

1.) Within 24 hours, leukocytes infiltrate the area of cell death. 2.) Enzymes are released from the dead cardiac cells (important indicators of MI). → Important in knowing if a MI occurred or how long ago it occurred. 3.) Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by second or third day. → This is when scar tissue starts to develop. 4.) Development of collateral circulation improves areas of poor perfusion. 5.) Necrotic zone identifiable by ECG changes and nuclear scanning. 6.) 10 to 14 days after MI, scar tissue is still weak and vulnerable to stress.

Complications of Myocardial Infarction (continued again)

Acute pericarditis: 1.) An inflammation of visceral and/or parietal pericardium. 2.) May result in cardiac compression, ↓ LV filling and emptying, heart failure. 3.) Pericardial friction rub may be heard on auscultation. 4.) Chest pain different from MI pain. → Pain in the chest that radiates to the back. → It is lessened when the patient sits down and gets worse when the patient lays down. → It is often confused with MI pain! → Not a medical emergency.

Location of Chest Pain (Angina)

All the different places that angina occurs!

Atherosclerosis

Atherosclerosis is a disease in which plaque builds up on the insides of your arteries: 1.) Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood that build up on the walls of your arteries. 2.) Over time, plaque hardens and narrows your arteries. 3.) The flow of oxygen-rich blood to your organs and other parts of your body is reduced. 4.) This can lead to serious problems, including heart attack, stoke, or even death (due to hypoxia). → Can lead to organ failure (kidney failure, liver failure, etc.). 5.) Can occur in any artery in the body but there is a preference for the coronary arteries.

Coronary Artery Disease and Acute Coronary Syndrome

Atherosclerosis is bad because it can lead to two different heart conditions: 1.) CAD - occurs when plaques builds up in the coronary arteries reducing and blocking blood flow to your heart tissue. This ischemia results in chest pain and may lead to a heart attack. → CAD also is called heart disease, and it's the leading cause of death in the United States. → Characterized by stable angina. 2.) ACS - is an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia. → Plaque instability, ulceration, and rupture. → Platelets accumulate and thrombus forms. → Increased narrowing or total occlusion of lumen. ⤷ STEMI (ST elevation MI). ⤷ NSTEMI (No ST elevation MI). ⤷ Unstable angnina.

Occlusion of the Left Anterior Descending Coronary Artery (most common area), Resulting in MI

Called "the widow maker."

ACS/MI Treatments

Coronary surgical revascularization: 1.) Coronary artery bypass graft (CABG) surgery. → Requires cardiopulmonary bypass (usually using lower extremity vessels). → Uses arteries and veins for grafts. 2.) Minimally invasive direct coronary artery bypass (MIDCAB). → Alternative to traditional CABG.

Complications of Myocardial Infarction (continued again and again)

Dressler syndrome: 1.) Characterized by pericarditis (similar type of pain to acute pericarditis) with effusion and fever that develop 4 to 6 weeks after MI. 2.) Pericardial (chest) pain. 3.) Pericardial friction rub may be heard on auscultation. 4.) Arthralgia (pain in joints not due to inflammation).

Chronic Stable Angina Nursing Management

Drug therapy: Goal: ↓O2 demand and/or ↑O2 supply. 1.) Nitrates (vasodialators increasing blood flow) - first line of defense. → Short-acting nitrates: Sublingual (heat or light). → Long-acting nitrates (usually an ointment of the chest or transdermal patch). ⤷ Nitroglycerin ointment. ⤷ Transdermal controlled-release nitroglycerin. 2.) β-Adrenergic blockers (decrease cardiac workload). → Good post MI. 3.) Calcium channel blockers. → If β-adrenergic blockers are poorly tolerated, contraindicated, or do not control anginal symptoms. → Used to manage Prinzmetal's angina. 4.) Angiotensin-converting enzyme inhibitors. If a patient stops exercising and the pain continues that means there is a more severe problem going on. A lethal arrhythmia may happen if their meds aren't working so it is important to get them on an ECG!

Coronary Artery Disease Defense Mechanisms

Inherent defense mechanism against coronary artery disease and plaque buildup. 1.) Collateral circulation: Normally some arterial anastomoses (or connections) exist within the coronary circulation. → When you artery starts to narrow, your body recognizes that parts of your body are not getting enough oxygenation. → It tries to find new pathways to form that can get oxygenation to that area of the body. → There is a genetic ability to do this and some do it better than others! 2.) Growth and extent of collateral circulation is attributed to two factors: → Inherited predisposition to develop new vessels (angiogenesis). → Presence of chronic ischemia. 3.) When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing.

Clinical Manifestations of ACS MI

Pain: 1.) Total occlusion → anaerobic metabolism and lactic acid accumulation → severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration. 2.) Described as heaviness, constriction, tightness, burning, pressure, or crushing. 3.) Common locations: substernal, retrosternal, or epigastric areas; pain may radiate.