Exam 2: Ch. 34 powerpoint CAD and ACS

Radial Artery Graft

-The radial artery is another conduit that can be used. -It is a thick muscular artery that is prone to spasm. Perioperative calcium channel blockers and long-acting nitrates can control the spasms. -Patency rates at 5 years are as high as 84%. There have been no reports of extremity complications (e.g., hand ischemia, wound infection) following the removal of this artery. *Teacher Comment* Other conduits include the gastroepiploic or inferior epigastric artery. However, they are rarely used as the dissection of these arteries is extensive. This increases the length of surgery and the risk for wound complications at the harvest site, especially in an obese or diabetic patient.

Myocardial InfarctionHealing Process

10 to 14 days after MI, scar tissue is still weak Myocardium vulnerable to stress Monitor patient carefully as activity level increases *Teacher Comment* At 10 to 14 days after MI, the new scar tissue is still weak. The myocardium is vulnerable to increased stress during this time because of the unstable state of the healing heart wall. It is also at this time that the patient's activity level may be increasing, so special caution and assessment are necessary. By 6 weeks after MI, scar tissue has replaced necrotic tissue and the injured area is considered healed.

Vessel occlusion with collateral circulation

A. Open, functioning coronary artery. B. Partial coronary artery closure with collateral circulation being established. C. Total coronary artery occlusion, with collateral circulation bypassing the occlusion to supply blood to the myocardium.

Collaborative and Nursing Management: CAD

Antiplatelet therapy -ASA -Clopidogrel (Plavix) *Teacher Comment* Unless contraindicated (e.g., history of GI bleeding), low-dose aspirin (81 mg) is recommended for most people at risk for CAD. Current recommendations include low-dose aspirin for men over 45 years and high-risk women (i.e., those with a calculated 10-year CAD risk of >20%) unless contraindicated. For high-risk women who are intolerant of aspirin, clopidogrel (Plavix) can be substituted. In healthy women 65 years or older, aspirin therapy should be considered if BP is controlled and the benefit for MI prevention outweighs the risk of GI bleed or hemorrhagic stroke.

Nursing Management Chronic Stable Angina and ACS

Acute intervention Semi-Fowler's position Supplemental oxygen Assess vital signs 12-lead ECG Administer a nitrate followed by an opioid analgesic, if needed Auscultate heart and breath sounds *Teacher Comment* If your patient experiences angina, institute the following measures: Position patient upright unless contraindicated and administer supplemental oxygen. Assess vital signs. Obtain a 12-lead ECG. Provide prompt pain relief first with a nitrate followed by an opioid analgesic if needed Auscultate heart and breath sounds. The patient will most likely be distressed and may have pale, cool, clammy skin. The BP and HR may be elevated. Auscultation of the heart may reveal an atrial (S4) or a ventricular (S3) gallop. A new murmur heard during an anginal attack may indicate ischemia of a papillary muscle of the mitral valve. The murmur is likely to be transient and disappear when symptoms stop. Ask the patient to describe the pain and to rate it on a scale of 0 to 10 before and after treatment to evaluate the effectiveness of the interventions. Supportive and realistic assurance and a calm approach help reduce the patient's anxiety during an anginal attack.

Nursing Management Chronic Stable Angina and ACS

Acute intervention Anxiety reduction Identify source and alleviate Patient teaching important Emotional and behavioral reaction Maximize patient's social support systems Consider open visitation *Teacher comment* Anxiety is present in all patients with ACS to some degree. Your role is to identify the source of anxiety and assist the patient in reducing it. If the patient is afraid of being alone, allow a caregiver to sit by quietly or check in with the patient frequently. For anxiety caused by lack of information, provide teaching based on the patient's stated need and level of understanding. Answer the patient's questions with clear, simple explanations. It is important to start teaching at the patient's level rather than to present a prepackaged program. For example, patients generally are not ready to learn about the pathology of CAD. The earliest questions usually relate to how the disease affects perceived control and independence. Examples include the following: When will I leave the intensive care unit? When can I be out of bed? When will I be discharged? When can I return to work? How many changes will I have to make in my life? Will this happen again? Frequently the patient may not be able to ask the most serious concern of ACS patients: Am I going to die? Even if a patient denies this concern, it is helpful for you to start conversation by remarking that fear of dying is a common concern among most patients who have experienced ACS. This gives the patient "permission" to talk about an uncomfortable and fearful topic. The emotional and behavioral reactions of a patient vary but frequently follow a predictable response pattern. Your role is to understand what the patient is currently experiencing and to support the use of constructive coping styles. Denial may be a positive coping style in the early phase of recovery from ACS. Assess the support structure of the patient and caregiver. Help to determine how you can help maximize the support system. Often the patient is separated from the most significant support system at the time of hospitalization. Your role can include talking with the caregiver(s), informing them of the patient's progress, allowing the patient and the caregiver to interact as necessary, and supporting the caregivers who will be able to provide the necessary support to the patient. Open visitation is helpful in decreasing anxiety and increasing support for the patient with ACS.

Nursing Management Chronic Stable Angina and ACS

Acute intervention Pain: nitroglycerin, morphine, oxygen Continuous monitoring ECG ST segment Heart and breath sounds VS, pulse oximetry, I&O Rest and comfort Balance rest and activity Begin cardiac rehabilitation *Teacher Comment* Priority interventions are aimed at decreasing the oxygen needs of a compromised myocardium and reducing the risk of complications. Provide NTG, morphine sulfate, and supplemental oxygen as needed to eliminate or reduce chest pain. Ongoing evaluation and documentation of the effectiveness of the interventions is important. Maintain continuous ECG monitoring while in the ED and intensive care unit and after transfer to a step-down or general unit. Dysrhythmias need to be identified quickly and treated. During the initial period after MI, ventricular fibrillation is the most common lethal dysrhythmia. In many patients, premature ventricular contractions or ventricular tachycardia precedes this dysrhythmia. Monitor the patient for the presence of reinfarction or ischemia by monitoring the ST segment for shifts above or below the baseline of the ECG. Silent ischemia can occur without clinical symptoms such as chest pain. Its presence places a patient at higher risk for adverse outcomes and even death. If you note ST segment changes, notify the physician. Perform a physical assessment to detect deviations from the patient's baseline findings. Assess heart and breath sounds and any evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). In addition to routine vital signs and pulse oximetry, monitor intake and output at least once a shift. It is important to promote rest and comfort with any degree of myocardial injury. Bed rest may be ordered for the first few days after an MI involving a large portion of the ventricle. A patient with an uncomplicated MI (e.g., angina resolved, no signs of complications) may rest in a chair within 8 to 12 hours after the event. The use of a commode or bedpan is based on patient preference. When sleeping or resting, the body requires less work from the heart than it does when active. It is important to plan nursing and therapeutic interventions to ensure adequate rest periods free from interruption. Comfort measures that can promote rest include a quiet environment, use of relaxation therapy (e.g., guided imagery), and assurance that staff are nearby and responsive to the patient's needs. Phase 1 of cardiac rehab occurs in the hospital. It is important that the patient understands the reasons why activity is limited but not completely restricted. Gradually increase the patient's cardiac workload through more demanding physical tasks so that the patient can achieve a discharge activity level adequate for home care. Phase 2 of rehab begins when the patient is discharged home and continues for 2 to 12 weeks. Phase 3 is long-term maintenance for optimal cardiac health.

Nursing ManagementAcute Coronary Syndrome

Ambulatory and home care Resumption of sexual activity Teach when discuss other physical activity Erectile dysfunction drugs contraindicated with nitrates Prophylactic nitrates before sexual activity When to avoid sex Typically 7-10 days post MI or when patient can climb two flights of stairs *Teacher Comment* It is important to include sexual counseling for cardiac patients and their partners. This often-neglected area of discussion may be difficult for both patients and HCPs to approach. However, the patient's concern about resumption of sexual activity after hospitalization for ACS often produces more stress than the physiologic act itself. The majority of these patients change their sexual behavior not because of physical problems, but because they are concerned about sexual inadequacy, death during intercourse, and impotence. A concerned and knowledgeable HCP could clarify the misconceptions held by these persons with specific counseling. Sexual activity for middle-aged men and women with their usual partners is no more strenuous than climbing two flights of stairs. It is helpful to consider sex as a physical activity and to discuss or explore feelings in this area when other physical activities are discussed. One helpful approach is, "Many people who have had a heart attack wonder when they will be able to resume sexual activity. Has this been of concern to you?" Another is, "If resuming sexual activity has been of concern to you, this information should be helpful." This type of nonthreatening statement brings up the topic, allows the patient to explore personal feelings, and gives the patient an opportunity to raise questions with you or another HCP. The patient needs to know that the inability to perform sexually after MI is common and that sexual dysfunction usually disappears after several attempts. Caution the patient that erectile dysfunction drugs are not to be used with nitrates because severe hypotension and even death have been reported. It is common for a patient who experiences chest pain on physical exertion to have some angina during sexual stimulation or intercourse. The patient may be instructed to take NTG prophylactically. It is also helpful to have the patient avoid sex soon after a heavy meal or after excessive ingestion of alcohol, when extremely tired or stressed, or with unfamiliar partners. Patients should also avoid anal intercourse because of the likelihood of eliciting a vasovagal response. Tell the patient that resumption of sex depends on the patient and his or her partner's emotional readiness and on the physician's assessment of the extent of recovery. It is generally safe to resume sexual activity 7 to 10 days after an uncomplicated MI. However, some physicians believe that the patient should decide when he or she is ready to resume sex. Others believe that a patient must be able to climb two flights of stairs briskly without dyspnea or chest pain before sexual activity is resumed. Provide the patient with reading material on resumption of sexual activity to facilitate discussion. Calmly and matter-of-factly introducing the subject of resumption of sexual activity during teaching about physical activity has positive effects of eliciting questions and concerns that might not have otherwise surfaced. For example, you might begin, "Sexual activity is like other forms of activity and should be gradually resumed after MI. If your ability to perform sexually is concerning you, the energy you use is no more than walking briskly or climbing two flights of stairs." This forms a factual basis for the patient to begin to seek information and explore personal feelings about resuming sex.

Coronary Artery Disease (CAD)

Atherosclerosis Begins as soft deposits of fat that harden with age Referred to as "hardening of arteries" Atheromas (fatty deposits) prefer coronary arteries Also known as ASHD, CVHD, IHD, CHD *Teacher Comment* Coronary artery disease is a type of blood vessel disorder that is included in the general category of atherosclerosis. The term atherosclerosis comes from two Greek words: athere, meaning "fatty mush," and skleros, meaning "hard." This combination indicates that atherosclerosis begins as soft deposits of fat that harden with age. Consequently, it is common to refer to atherosclerosis as "hardening of the arteries." Although this condition can occur in any artery in the body, the atheromas (fatty deposits) prefer the coronary arteries. The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary heart disease, and CAD all describe this disease process.

Coronary Artery Disease Etiology and Pathophysiology

Atherosclerosis is the major cause of CAD Characterized by lipid deposits within intima of artery Endothelial injury and inflammation play a major role in development *Teacher Comment* Atherosclerosis is the major cause of CAD. It is characterized by deposits of lipids within the intima of the artery. Endothelial injury and inflammation play a central role in the development of atherosclerosis.

Myocardial Infarction Healing Process

By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed, but less compliant Ventricular remodeling Normal myocardium will hypertrophy and dilate in an attempt to compensate for the infarcted muscle *Teacher comment* The scarred area is often less compliant than the surrounding area. This condition may be manifested by uncoordinated wall motion, ventricular dysfunction, altered conduction patterns, or heart failure. These changes in the infarcted muscle also cause changes in the unaffected myocardium as well. In an attempt to compensate for the damaged muscle, the normal myocardium will hypertrophy and dilate. This process is called ventricular remodeling. Remodeling of normal myocardium can lead to the development of late heart failure (HF), especially in the individual with atherosclerosis of other coronary arteries and/or an anterior MI.

Coronary Artery Disease Etiology and Pathophysiology (continue)

C-reactive protein (CRP) Nonspecific marker of inflammation Increased in many patients with CAD Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol *teacher Comment* C-reactive protein (CRP), a protein produced by the liver, is a nonspecific marker of inflammation. It is increased in many patients with CAD. The level of CRP rises when there is systemic inflammation. Chronic elevations of CRP are associated with unstable plaques and the oxidation of low-density lipoprotein (LDL) cholesterol, further contributing to atherosclerosis.

Nursing ManagementAcute Coronary Syndrome

CABG: postoperative nursing care Assess patient for bleeding Monitor hemodynamic status Assess fluid status Replace electrolytes PRN Restore temperature Monitor for atrial fibrillation (which is common) *Teacher Comment* Focus your nursing care on Assessing the patient for bleeding (e.g., chest tube drainage, incision sites) Hemodynamic monitoring Checking fluid status Replacing electrolytes as needed Restoring temperature (e.g., warming blankets) Postoperative dysrhythmias, specifically atrial dysrhythmias, are common in the first 3 days after CABG surgery. Postoperative atrial fibrillation (AF) occurs in 20% to 50% of patients. Beta blockers should be restarted as soon as possible after surgery (unless contraindicated) to reduce the incidence of AF.

He develops chest pain and ST-segment depression during an exercise stress test. What additional testing would you expect M.P. to undergo at this point?

Cardiac Catheterization

Clinical Manifestations of ACS Myocardial Infarction

Cardiovascular Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) Crackles Jugular venous distention Abnormal heart sounds S3 or S4 New murmur *Teacher Comment* In response to the release of catecholamines, BP and HR may initially increase. The BP may later drop because of decreased cardiac output (CO). If severe enough, this may result in decreased renal perfusion and urine output. Crackles, if present, may persist for several hours to several days, suggesting left ventricular dysfunction. Jugular venous distention, hepatic engorgement, and peripheral edema may indicate right ventricular dysfunction. Cardiac examination may reveal abnormal heart sounds that may seem distant. Other abnormal sounds suggesting ventricular dysfunction are S3 and S4. In addition, a loud holosystolic murmur may develop and may indicate a septal defect, papillary muscle rupture, or valve dysfunction.

Clinical Manifestations of ACS Myocardial Infarction

Catecholamine release - stimulation of SNS Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch *Teacher Comment* During the initial phase of MI, the ischemic myocardial cells release catecholamines (norepinephrine and epinephrine) that are normally found in these cells. This results in release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels. On physical examination, the patient's skin may be ashen, clammy, and cool to touch.

Based on the presence of these risk factors and M.P.'s complaints of "indigestion" associated with activity, what type of angina is M.P. likely experiencing?

Chronic stable angina

Coronary Artery Disease Etiology Pathophysiology (Continue)

Collateral circulation Arterial anastomoses (or connections) within the coronary circulation Increased with chronic ischemia May be inadequate with rapid-onset CAD *Teacher Comment* Normally some arterial anastomoses or connections, termed collateral circulation, exist within the coronary circulation. Two factors contribute to the growth and extent of collateral circulation: (1) the inherited predisposition to develop new blood vessels (angiogenesis) and (2) the presence of chronic ischemia. When a plaque occludes the normal flow of blood through a coronary artery and the resulting ischemia is chronic, increased collateral circulation develops. When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing, and the myocardium may still receive an adequate amount of blood and oxygen. However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or coronary spasm, time is inadequate for collateral development. Consequently, a diminished blood flow results in a more severe ischemia or infarction.

Nursing ManagementAcute Coronary Syndrome

Complications related to CPB Bleeding and anemia from damage to RBCs and platelets Fluid and electrolyte imbalances Hypothermia as blood is cooled as it passes through the bypass machine Infections *Teacher Comment* Many of the postoperative complications that develop after CABG surgery relate to the use of CPB. Major consequences of CPB are systemic inflammation, which includes complications of Bleeding and anemia from damage to red blood cells and platelets Fluid and electrolyte imbalances Hypothermia as blood is cooled as it passes through the CPB machine Infections

Unstable Angina and MIDiagnostic Studies

Coronary angiography Exercise or pharmacologic stress testing Echocardiogram *Teacher Comment* Coronary Angiography The patient with UA or NSTEMI may or may not undergo coronary angiography to evaluate the extent of the disease. Guidelines suggest that it is reasonable to do coronary angiography on stable but high-risk patients with UA/NSTEMI. If appropriate, a PCI is performed at this time. Some patients may be treated with conservative medical management. Coronary angiography is the only way to confirm the diagnosis of Prinzmetal's angina. Exercise or pharmacologic stress testing and echocardiogram are used when a patient has an abnormal but nondiagnostic baseline ECG. A dobutamine (Dobutrex), dipyridamole (Persantine), or adenosine (Adenocard) stress echocardiogram stimulates the effects of exercise and is used in patients unable to exercise.

M.P.'s ECG demonstrates significant ST elevation. What evidence-based intervention would you expect to prepare M.P. to undergo within 90 minutes of arrival to the ED?

Coronary revascularization with emergent PCI (if available) If not available, administration of thrombolytic agents

Unstable Angina and MIDiagnostic Studies

Detailed health history 12-lead ECG -Changes in QRS complex, ST segment, and T wave -Distinguish between STEMI and NSTEMI -Pathologic Q wave *Teacher Comment* In addition to the patient's history of pain, risk factors, and health history, the primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac marker. The ECG is one of the primary diagnostic tools. Changes in the QRS complex, ST segment, and T wave caused by ischemia and infarction can develop quickly with UA and MI. For diagnostic and treatment purposes, it is important to distinguish between STEMI and UA or NSTEMI. Patients with STEMI tend to have a more extensive MI that is associated with prolonged and complete coronary occlusion, and the development of a pathologic Q wave on the ECG. Patients with UA or NSTEMI usually have transient thrombosis or incomplete coronary occlusion and usually do not develop pathologic Q waves. Because MI is a dynamic process that evolves with time, the ECG often reveals the time sequence of ischemia, injury, infarction, and resolution of the infarction. The ECG must be read very carefully as there can be very subtle changes at first. It may also be normal or nondiagnostic when the patient comes to the ED with a complaint of chest pain. Within a few hours, the ECG may change to reflect the infarction process. For this reason, when the initial 12-lead ECG is nondiagnostic, serial 12-lead ECGs are done.

Sudden Cardiac Death Nursing/Collaborative Management

Diagnostic workup to rule out or confirm MI Cardiac markers ECGs Treat accordingly Cardiac catheterization PCI or CABG *Teacher Comment* People who survive an episode of SCD require a diagnostic workup to determine whether they have had an MI. Thus serial analysis of cardiac markers and ECGs are done, and the patient is treated accordingly. In addition, because most persons with SCD have CAD, cardiac catheterization is indicated to determine the possible location and extent of coronary artery occlusion. PCI or CABG surgery may be indicated.

Cardiopulmonary Bypass

During CPB, blood is diverted from the patient's heart to a machine where it is oxygenated and returned (via a pump) to the patient. This allows the surgeon to operate on a quiet, nonbeating, bloodless heart while perfusion to vital organs is maintained.

Collaborative CareAcute Coronary Syndrome

Drug therapy IV nitroglycerin Morphine sulfate β-adrenergic blockers Angiotensin-converting enzyme inhibitors Antidysrhythmia drugs Cholesterol-lowering drugs Stool softeners *Teacher Comment* IV NTG (Tridil) is used in the initial treatment of the patient with ACS. The goal of therapy is to reduce anginal pain and improve coronary blood flow. IV NTG decreases preload and afterload while increasing the myocardial oxygen supply. The onset of action is immediate. Titrate NTG to control and stop chest pain. Because hypotension is a common side effect, BP is closely monitored during this time. Patients who do become hypotensive are often volume depleted and can benefit from an IV fluid bolus. Morphine sulfate is the drug of choice for chest pain that is unrelieved by NTG. As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility, and decreasing BP and HR. In addition, morphine can help reduce anxiety and fear. In rare situations, morphine can depress respirations. Monitor patients for signs of bradypnea or hypotension, conditions to avoid in myocardial ischemia and infarction. β-adrenergic blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility. The use of these drugs in patients who are not at risk for complications of MI (e.g., cardiogenic shock) reduces the risk of reinfarction and the occurrence of HF. The continuation of β-adrenergic blockers indefinitely is recommended. ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI with an EF of 40% or less. The use of ACE inhibitors can help prevent ventricular remodeling and prevent or slow the progression of HF. For patients who cannot tolerate ACE inhibitors, angiotensin II receptor blockers should be considered. Dysrhythmias are the most common complications after an MI. In general, they are self-limiting and are not treated aggressively unless they are life threatening (e.g., sustained ventricular tachycardia). A lipid panel is obtained on all patients admitted with ACS. All patients with elevated triglycerides and LDL cholesterol should receive lipid-lowering drugs. After an MI, the patient may be predisposed to constipation because of bed rest and opioid administration. Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate bowel movements. This prevents straining and the resultant vagal stimulation from the Valsalva maneuver. Vagal stimulation produces bradycardia and can provoke dysrhythmias.

Chronic Stable Angina Collaborative Care

Goal: ↓ O2 demand and/or ↑ O2 supply Short-acting nitrates Dilate peripheral and coronary blood vessels Give sublingually (tablet) or by spray If no relief in 5 minutes, call EMS; if some relief ,repeat every 5 minutes for maximum 3 doses Patient teaching Can use prophylactically *Teacher Comment* The treatment of chronic stable angina aims to decrease oxygen demand and/or increase oxygen supply. Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by: 1. Dilating peripheral blood vessels. This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial oxygen demand is decreased because of the reduced cardiac workload. 2. Dilating coronary arteries and collateral vessels. This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is difficult to achieve Nitroglycerin (NTG) given sublingually (Nitrostat) or by translingual spray (Nitrolingual) will usually relieve pain in about 3 minutes and has a duration of approximately 30 to 60 minutes. The recommended dose for the patient for whom NTG has been prescribed is one tablet taken sublingually (SL) or one metered spray for symptoms of angina. If symptoms are unchanged or worse after 5 minutes, the patient should contact the emergency medical services (EMS) system before taking additional NTG. If symptoms are significantly improved by one dose of NTG, instruct the patient or caregiver to repeat NTG every 5 minutes for a maximum of three doses and contact EMS if symptoms have not resolved completely. Instruct the patient in the proper use of NTG. It should be easily accessible to the patient at all times. The patient should store the tablets away from light and heat sources, including body heat, to protect from degradation. Tablets are packaged in light-resistant bottles with metal caps. Once opened, the tablets tend to lose potency and should be replaced every 6 months. Tell the patient to place a NTG tablet under the tongue and allow it to dissolve. If using the spray, it should be directed on or under the tongue, not inhaled. NTG should cause a tingling sensation when administered; otherwise it may be outdated. Warn the patient that a headache, dizziness, or flushing may occur. Caution the patient to change positions slowly after NTG use because orthostatic hypotension may occur. Patients can use NTG prophylactically before undertaking an activity that is known to cause an anginal attack. In these cases, the patient can take a tablet 5 to 10 minutes before beginning the activity. Instruct the patient to report any changes in the usual pattern of pain, especially increasing frequency or nocturnal angina, to the HCP.

Complications of Myocardial Infarction

Heart failure -Occurs when the pumping power of the heart has diminished -Can be subtle or severe Cardiogenic shock -Occurs because of severe LV failure -Requires aggressive management *Teacher Comment* Heart failure is a complication that occurs when the pumping action of the heart is reduced. Depending on the severity and extent of the injury, HF occurs initially with subtle signs such as mild dyspnea, restlessness, agitation, or slight tachycardia. Other signs indicating the onset of HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds on auscultation, crackles on auscultation of breath sounds, and jugular vein distention. Cardiogenic shock occurs when oxygen and nutrients supplied to the tissues are inadequate because of severe left ventricular failure. This occurs less often with the early and rapid treatment of MI with PCI or thrombolytic therapy. When cardiogenic shock does occur, it has a high mortality rate. Cardiogenic shock requires aggressive management. This includes control of dysrhythmias, intraaortic balloon pump (IABP) therapy, and support of contractility with the use of vasoactive drugs. The goal of therapy is to maximize oxygen delivery, reduce oxygen demand, and prevent complications such as acute renal failure.

Gerontologic ConsiderationsCAD

Increased incidence and mortality associated with CAD in older adults Strategies to reduce risk and treat CAD are effective Treat hypertension, ↑lipids Smoking cessation *Teacher Comment* The incidence of cardiac disease is greatly increased in older adults and is the leading cause of death in older persons. In the older adult, CAD is often a result of the complex interaction of nonmodifiable risk factors (e.g., age) and lifelong modifiable risk behaviors (e.g., inactivity, tobacco use). Strategies to reduce CAD risk and to treat CAD are effective in this age-group. Aggressive treatment of hypertension and hyperlipidemia will stabilize plaques in the coronary arteries of older adults, and cessation of tobacco use helps decrease the risk for CAD at any age.

Clinical Manifestations of CAD Chronic Stable Angina

Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms 5 to 15 minute duration ST segment depression and/or T-wave inversion Control with drugs *Teacher Comment* Chronic stable angina refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms. The pain usually lasts for only a few minutes (5 to 15 minutes) and commonly subsides when the precipitating factor is resolved. Pain at rest is unusual. A 12-lead electrocardiogram (ECG) often shows ST segment depression and/or T-wave inversion indicating ischemia. The ECG will return to baseline when the pain is relieved. Chronic stable angina is controlled with drugs on an outpatient basis. Because chronic stable angina is often predictable, drugs are timed to provide peak effects during the time of day when angina is likely to occur. For example, if angina occurs when rising, the patient can take the drug as soon as awakening and wait 30 minutes to 1 hour before engaging in activity.

Chronic Stable Angina Collaborative Care

Long-acting nitrates -To reduce angina incidence Main side effects: headache, orthostatic hypotension Methods of administration Oral Nitroglycerin (NTG) ointment Transdermal controlled-release NTG *Teacher Comment* Long-acting nitrates are used to reduce the incidence of anginal attacks. The main side effect of all nitrates is headache from the dilation of cerebral blood vessels. Advise patients to take acetaminophen (Tylenol) with their nitrate to relieve the headache. Over time, the headaches may decrease but the antianginal effect is still present. Orthostatic hypotension is a complication of all nitrates. You should monitor BP after the initial dose as the venous dilation that occurs may cause a drop in BP, especially in volume-depleted patients. To limit this, patients are often scheduled an 8-hour nitrate-free period every day, usually during the night, unless the patient experiences nocturnal angina. Finally, tolerance to NTG-induced vasodilation can develop. Can be given orally, such as isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur), Nitropaste is a 2% NTG topical ointment dosed by the inch. It is placed on the upper body or arm, over a flat muscular area that is free of hair and scars. Once absorbed, it produces anginal prophylaxis for 3 to 6 hours. It is especially useful for nocturnal and unstable angina. Transdermal NTG drug administration offers the advantage of steady plasma levels within the therapeutic range during 24 hours, thus making only one application a day necessary.

Risk Factors for CAD

Modifiable risk factors Psychologic states Homocysteine level Substance abuse *Teacher Comment* *Psychologic States* The Framingham study provided early evidence that certain behaviors and lifestyles contribute to the development of CAD. One type of behavior, referred to as type A, includes perfectionism and a hardworking, driving personality. The type A person often suppresses anger and hostility, has a sense of time urgency, is impatient, and often creates stress and tension. This person may be more prone to MIs than a type B person, who is more easygoing, takes upsets in stride, knows personal limitations, takes time to relax, and is not an overachiever. However, findings from studies regarding these relationships are inconsistent. Studies now are focusing on specific psychologic risk factors thought to increase risk of CAD. These include depression, acute and chronic stress (e.g., poverty, serving as a caregiver), anxiety, hostility and anger, and lack of social support. In particular, depression is a risk factor for both the development and worsening of CAD. Depressed patients have elevated levels of circulating catecholamines that may contribute to endothelial injury and inflammation and platelet activation. More research on the treatment of depression and other negative psychologic states (e.g., anger) in patients with or at risk for CAD is needed to improve the emotional and physical health of these patients. Stressful states do correlate with the development of CAD. Sympathetic nervous system (SNS) stimulation and its effect on the heart are the physiologic mechanism by which stress predisposes to the development of CAD. SNS stimulation causes an increased release of catecholamines (i.e., epinephrine, norepinephrine). This stimulation increases HR and intensifies the force of myocardial contraction, resulting in increased myocardial oxygen demand. Also, stress-induced mechanisms can cause elevated lipid and glucose levels and changes in blood coagulation, which can lead to increased atherogenesis. *Homocysteine* High blood levels of homocysteine have been linked to an increased risk for CAD and other cardiovascular diseases. Homocysteine is produced by the breakdown of the essential amino acid methionine, which is found in dietary protein. High homocysteine levels possibly contribute to atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque buildup, and (3) altering the clotting mechanism to make clots more likely to occur. B-complex vitamins (B6, B12, folic acid) have been shown to lower blood levels of homocysteine. Generally, a screening test for homocysteine is limited to those suspected of having elevated levels, such as older patients with pernicious anemia or people who develop CAD at an early age. *Substance Abuse* The use of illicit drugs, such as cocaine and methamphetamine, can produce coronary spasm resulting in myocardial ischemia and chest pain. Most people who are seen in the ED with drug-induced chest pain are initially indistinguishable from those with CAD. Although MI can occur, these patients more often have sinus tachycardia, high BP, angina, and anxiety.

Chronic Stable Angina Types of Angina

Microvascular angina Chest pain occurs in the absence of significant coronary atherosclerosis or coronary spasm Myocardial ischemia associated with abnormalities of the coronary microcirculation Coronary microvascular disease (MVD) affects small, distal coronary arteries *Teacher Comment* In microvascular angina, chest pain occurs in the absence of significant coronary atherosclerosis or coronary spasm, especially in women. In these patients, chest pain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation. This is known as coronary microvascular disease (MVD). Coronary MVD affects the small branches of the distal coronary arteries, whereas CAD affects larger coronary arteries. In coronary MVD, plaque can be diffuse, evenly distributed, or develop as blockages in the tiny coronary arteries. Prevention and treatment of coronary MVD follows the same recommendations as for CAD.

Clinical Manifestations of ACS Myocardial Infarction

Nausea and vomiting Reflex stimulation of the vomiting center by severe pain Vasovagal reflex Fever Up to 100.4° F (38° C) in first 24 hours Systemic inflammatory process caused by myocardial cell death *Teacher Comment* The patient may experience nausea and vomiting. These symptoms can result from reflex stimulation of the vomiting center by the severe pain. They can also result from vasovagal reflexes initiated from the area of the infarcted myocardium. The temperature may increase within the first 24 hours up to 100.4° F (38° C). The temperature elevation may last for as long as 1 week. This increase in temperature is due to a systemic inflammatory process caused by myocardial cell death.

Nursing ManagementChronic Stable Angina and ACS

Nursing assessment: subjective data Health history CAD/chest pain/angina/ MI Valve disease Heart failure/cardiomyopathy, Hypertension, diabetes, anemia, lung disease, hyperlipidemia Drugs History of present illness *teacher comment* Obtain the following health information from the client: Past health history: Previous history of CAD, chest pain/angina, MI, valve disease (e.g., aortic stenosis), heart failure, or cardiomyopathy; hypertension, diabetes, anemia, lung disease; hyperlipidemia Drugs: Use of antiplatelets/anticoagulants, nitrates, angiotensin-converting enzyme inhibitors, β-adrenergic blockers, calcium channel blockers; antihypertensive drugs; lipid-lowering drugs; over-the-counter drugs (e.g., vitamin and herbal supplements) History of present illness: Description of events related to current illness, including any self-treatments and response

Clinical Manifestations of ACS Myocardial Infarction

Pain Described as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms *Teacher Comment* It may occur while the patient is active or at rest, or asleep or awake. However, it commonly occurs in the early morning hours. It usually lasts for 20 minutes or longer and is more severe than usual anginal pain. Not everyone has classic symptoms. Some patients may not experience pain but may have "discomfort," weakness, or shortness of breath. Although women and men have more similarities than differences in their symptoms of an acute MI, some women may experience atypical discomfort, shortness of breath, or fatigue.

Complications of Myocardial Infarction

Papillary muscle dysfunction -Causes mitral valve regurgitation -Aggravates an already compromised LV → rapid clinical deterioration Ventricular aneurysm -Myocardial wall becomes thinned and bulges out during contraction -Leads to HF, dysrhythmias, and angina *Teacher Comment* Papillary muscle dysfunction may occur if the infarcted area includes or is near the papillary muscle that attaches to the mitral valve. Papillary muscle rupture is a rare and life-threatening complication. It causes massive mitral valve regurgitation. Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium. This condition aggravates an already damaged left ventricle by reducing CO even further. There is rapid clinical deterioration of the patient. Treatment includes rapid afterload reduction with nitroprusside (Nipride) and/or IABP therapy, and immediate cardiac surgery with mitral valve repair or replacement. Ventricular aneurysm results when the infarcted myocardial wall is thin and bulges out during contraction. This can develop within a few days, weeks, or months. The patient with a ventricular aneurysm may experience HF, dysrhythmias, and angina. Besides ventricular rupture, which is fatal, ventricular aneurysms harbor thrombi that can lead to an embolic stroke.

Collaborative and Nursing Management: CAD

Physical fitness FITT formula: 30 minutes most days plus weight training 2 days a week Regular physical activity contributes to Weight reduction Reduction of >10% in systolic BP In some men more than women, increase in HDL cholesterol *Teacher Comment* Physical Activity A physical activity program should be designed to improve physical fitness by following the FITT formula: Frequency (how often) Intensity (how hard) Type (isotonic) Time (how long) Everyone should aim for at least 30 minutes of moderate physical activity on most days of the week. In addition, adding weight training to an exercise program 2 days a week can help treat metabolic syndrome and improve muscle strength. Examples of moderate physical activity include brisk walking, hiking, biking, and swimming. Regular physical activity contributes to weight reduction, reduction in systolic BP, and, in some men more than women, an increase in HDL cholesterol.

Nursing Management Chronic Stable Angina and ACS

Planning: overall goals Relief of pain Preservation of myocardium Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors *Teacher Comment* The overall goals for a patient with ACS include (1) relief of pain, (2) preservation of myocardium, (3) immediate and appropriate treatment, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors.

Clinical Manifestations of CAD Angina

Pressure/ache Squeezing, heavy, choking, or suffocating sensation Rarely sharp or stabbing Indigestion or burning Various locations *Teacher Comment* When questioned, some patients may deny feeling pain but will describe a pressure or ache in the chest. It is an unpleasant feeling, often described as a squeezing, heavy, choking, or suffocating sensation. Angina is rarely sharp or stabbing, and it usually does not change with position or breathing. Many people with angina complain of indigestion or a burning sensation in the epigastric region. Although most of the pain experienced by people with angina appears substernally, the sensation may occur in the neck or may radiate to various locations, including the jaw and shoulders, and down the arms. Often people will complain of pain between the shoulder blades and will dismiss it as not being heart related.

Chronic Stable AnginaTypes of Angina

Prinzmetal's (variant) angina Occurs at rest due to spasm of a major coronary artery May occur with or without CAD Not precipitated by increased demand Chest pain with marked, transient ST-segment elevation *Teacher Comment* Prinzmetal's angina (variant angina) often occurs at rest, usually in response to spasm of a major coronary artery. The spasm may occur in the absence or presence of CAD. Prinzmetal's angina is not usually precipitated by increased physical demand. Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium. Factors causing coronary artery spasm include increased myocardial oxygen demand and increased levels of certain substances (e.g., tobacco smoke, alcohol, amphetamines). When spasm occurs, the patient experiences angina and transient ST-segment elevation.

clinical manefestation of CAD angina

Progressive disease O2 demand > O2 supply → myocardial ischemia Angina = reversible ischemia Occurs when arteries are blocked 75% or more Hypoxic within 10 seconds of occlusion Viable for 20 minutes *Teacher Comment* CAD is a progressive disease, and patients may be asymptomatic for many years or they may develop chronic stable chest pain. When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen, myocardial ischemia occurs. Angina, or chest pain, is the clinical manifestation of reversible myocardial ischemia. Either an increased demand for oxygen or a decreased supply of oxygen can lead to myocardial ischemia. The primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis. For ischemia secondary to atherosclerosis to occur, the artery is usually blocked (stenosed) 75% or more. On the cellular level, the myocardium becomes hypoxic within the first 10 seconds of coronary occlusion. In ischemic conditions, cardiac cells are viable for approximately 20 minutes. With restoration of blood flow, aerobic metabolism resumes, contractility is restored, and cellular repair begins.

Clinical Manifestations of ACS Myocardial Infarction (MI)

Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) 80%-90% secondary to thrombus Ischemia starts in subendocardium Necrosis of entire thickness of myocardium takes 4 to 6 hours Loss of contractile function *Teacher Comment* A myocardial infarction (MI) occurs because of sustained ischemia, causing irreversible myocardial cell death (necrosis). Thrombus formation causes 80% to 90% of all acute MIs. When a thrombus develops, blood to the myocardium distal to the blockage is halted, resulting in necrosis. The acute MI process takes time. Cardiac cells can withstand ischemic conditions for approximately 20 minutes before cellular death begins. The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the cardiac muscle). If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness of the heart muscle to become necrosed. If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as 12 hours. Contractile function of the heart stops in the necrotic area(s). The degree of altered function depends on the area of the heart involved and the size of the infarction.

Collaborative CareAcute Coronary Syndrome

STEMI or NSTEMI with + cardiac markers → reperfusion therapy Emergent PCI -Treatment of choice for confirmed MI -Goal: 90 minutes from door to catheter laboratory -Balloon angioplasty + drug-eluting stent(s) -Many advantages over CABG *Teacher Comment* For patients with STEMI or NSTEMI with positive cardiac markers, reperfusion therapy is initiated. Reperfusion therapy can include emergent PCI for STEMI and NSTEMI or thrombolytic (fibrinolytic) therapy for STEMI. The goal in the treatment of MI is to salvage as much myocardial muscle as possible. Emergent PCI is the first line of treatment for patients with confirmed MI (i.e., definitive ECG changes and/or positive cardiac markers). The goal is to open the blocked artery within 90 minutes of arrival to a facility that has an interventional cardiac catheterization laboratory. In this situation, the patient will undergo a cardiac catheterization to locate the blockage(s), assess the severity of the blockage(s), determine the presence of collateral circulation, and evaluate left ventricular function. During the procedure, treatment modalities (e.g., placement of drug-eluting stents) are selected. Patients with severe left ventricular dysfunction may require the addition of intraaortic balloon pump (IABP) therapy, and a small percentage of patients may require emergent CABG surgery. The advantages of PCI include the following: (1) it provides an alternative to surgical intervention; (2) it is performed with local anesthesia; (3) the patient is ambulatory shortly after the procedure; (4) the length of hospital stay is approximately 1 to 3 days compared with the 4- to 6-day stay with CABG surgery, thus reducing hospital costs; and (5) the patient can return to work several weeks sooner after PCI compared to 6- to 8-week convalescence after CABG. Advances in PCI techniques have significantly reduced the need for emergent CABG. Currently, there are more PCIs performed than CABGs.

Serum Cardiac Markers After MI

Serum cardiac markers are proteins released into the blood from necrotic heart muscle after an MI. These markers are important in the diagnosis of MI. The onset, peak, and duration of levels of these markers are shown in this graph. Cardiac-specific troponin has two subtypes: cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI). These markers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase (CK)-MB. Serum levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days. CK levels begin to rise at about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours. The CK enzymes are fractionated into bands. The CK-MB band is specific to myocardial cells and also helps quantify myocardial damage. Myoglobin is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours. Although it is one of the first serum cardiac markers to appear after an MI, it lacks cardiac specificity. Its role in diagnosing MI is limited.

Chronic Stable Angina Types of Angina

Silent ischemia Ischemia that occurs in the absence of any subjective symptoms Associated with diabetic neuropathy Confirmed by ECG changes *Teacher Comment* Silent ischemia refers to ischemia that occurs in the absence of any subjective symptoms. Patients with diabetes have an increased prevalence of silent ischemia. This is most likely due to diabetic neuropathy affecting the nerves that innervate the cardiovascular system. Silent ischemia is documented by ECG changes.

Stages of Atherosclerosis

The endothelium (the inner lining the vessel wall) is normally nonreactive to platelets and leukocytes, as well as coagulation, fibrinolytic, and complement factors. However, the endothelial lining can be injured as a result of tobacco use, hyperlipidemia, hypertension, toxins, diabetes, hyperhomocysteinemia, and infection causing a local inflammatory response. CAD is a progressive disease that develops over many years. When it becomes symptomatic, the disease process is usually well advanced. The stages of development in atherosclerosis are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion. *B. Fatty Streak* Fatty streaks, the earliest lesions of atherosclerosis, are characterized by lipid-filled smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow tinge appears. Fatty streaks can be seen in the coronary arteries by age 15 and involve an increasing amount of surface area as one ages. *C. Fibrous Plaque* The fibrous plaque stage is the beginning of progressive changes in the endothelium of the arterial wall. These changes can appear in the coronary arteries by age 30 and increase with age. Once endothelial injury has taken place, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intima. Collagen covers the fatty streak and forms a fibrous plaque with a grayish or whitish appearance. These plaques can form on one portion of the artery or in a circular fashion involving the entire lumen. The result is a narrowing of the vessel lumen and a reduction in blood flow to the distal tissues. *D. Complicated Lesion* The final stage in the development of the atherosclerotic lesion is the most dangerous. As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration, and rupture. Once the integrity of the artery's inner wall is compromised, platelets accumulate in large numbers, leading to a thrombus. The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery. At this stage, the plaque is referred to as a complicated lesion.

Acute Coronary Syndrome

When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops and encompasses the spectrum of unstable angina (UA), non-ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI). Although each remains a distinct diagnosis, this nomenclature (ACS) reflects the relationships among these disorders.

Myocardial InfarctionHealing Process

Within 24 hours, leukocytes infiltrate the area of cell death Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day → thin wall Necrotic zone identifiable by ECG changes and nuclear scanning Collagen matrix laid down *Teacher Comment* The body's response to cell death is the inflammatory process. Within 24 hours, leukocytes infiltrate the area of cell death. The proteolytic enzymes of the neutrophils and macrophages begin to remove necrotic tissue by the fourth day. During this time, the necrotic muscle wall is thin. The necrotic zone is identifiable by ECG changes (e.g., ST-segment elevation, pathologic Q wave) and by nuclear scanning after the onset of symptoms. At this point, the neutrophils and monocytes have cleared the necrotic debris from the injured area, and the collagen matrix that will eventually form scar tissue is laid down.

Which patient is most at risk for developing coronary artery disease? a. A hypertensive patient who smokes cigarettes b. An overweight patient who uses smokeless tobacco c. A patient who has diabetes and uses methamphetamines d. A sedentary patient who has elevated homocysteine levels

a. A hypertensive patient who smokes cigarettes

saturated, monounsaturated, polyunsaturated

saturated= bad monounsaturated=ok polyunsaturated=great!

Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are a. Obesity and smokeless tobacco use. b. Hypertension and cigarette smoking. c. Elevated serum lipids and diabetes mellitus. d. Physical inactivity and elevated homocysteine levels.

b. hypertension and cigarette smoking

The nurse is caring for a patient who survived a sudden cardiac death. What should the nurse include in the discharge instructions? a. "Because you responded well to CPR, you will not need an implanted defibrillator." b. "Your family members should learn how to perform CPR and practice these skills regularly." c. "The most common way to prevent another arrest is to take your prescribed drugs." d. "Since there was no evidence of a heart attack, you do not need to worry about another episode

b. your family members should learn how to perform CPR and practice these skills regularly

The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective when the patient says, a. "I should not eat any red meat such as beef, pork, or lamb." b. "I should have some type of fish at least 3 times a week." c. "Most of my fat intake should be from olive oil or the oils in nuts." d. "If I reduce the fat in my diet to about 5% of my calories, I will be much healthier."

c. "Most of my fat intake should be from olive oil or the oils in nuts

A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation. When reviewing the health care provider's admission orders, which order should the nurse question? a. Oxygen at 4 L/min per nasal cannula b. Morphine sulfate 2 mg IV every 10 minutes until the pain is relieved c. Tissue plasminogen activator (t-PA) 100 mg IV infused over 3 hours d. IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3 to 5 minutes

c. tissue plasminogen activator *t-PA) 100 mg IV infused over 3hrs

Complications of Myocardial Infarction

Acute pericarditis -An inflammation of visceral and/or parietal pericardium -May result in cardiac tamponade, ↓ LV filling and emptying, heart failure -Chest pain -Pericardial friction rub -ECG changes -Treated with antiinflammatory agents *Teacher Comment* Pericarditis is an inflammation of the visceral and/or parietal pericardium May result in cardiac tamponade, decreased ventricular filling and emptying, and HF. It occurs 2 to 3 days after an acute MI as a common complication of the infarction. Chest pain, which may vary from mild to severe, and is aggravated by inspiration, coughing, and movement of the upper body, characterizes pericarditis. Sitting in a forward position often relieves the pain. Assess the patient with suspected pericarditis for the presence of a friction rub over the pericardium. Fever may also be present. There may be hypotension and/or a narrow pulse pressure associated with decreased LV filling and emptying. Diagnosis of pericarditis can be made with serial 12-lead ECGs. Typical ECG changes include diffuse ST-segment elevations. This reflects the inflammation of the pericardium. Treatment includes pain relief with NSAIDs, aspirin, or corticosteroids.

Nursing Management Chronic Stable Angina and ACS

Ambulatory and home care Provide reassurance Patient teaching CAD and angina Precipitating factors for angina Risk factor reduction Drugs *Teacher Comment* The patient with a history of angina should be reassured that a long, active life is possible. Prevention of angina is preferable to its treatment, and this is where teaching is important. You need to provide the patient with information regarding CAD, angina, precipitating factors for angina, risk factor reduction, and drugs. Give the patient instructions on how to avoid or control precipitating factors. For example, teach the patient to avoid exposure to extremes of weather and the consumption of large, heavy meals. If a heavy meal is eaten, instruct the patient to rest for 1 to 2 hours after the meal because blood is shunted to the GI tract to aid digestion and absorption. Assist the patient to identify personal risk factors for CAD. Once known, discuss the various methods of decreasing any modifiable risk factors with the patient. Teach the patient and caregiver about diets that are low in salt and saturated fats. Maintaining ideal body weight is important in controlling angina because excess weight increases myocardial workload. Adhering to a regular, individualized program of physical activity that conditions rather than overstresses the heart is important. For example, advise patients to walk briskly on a flat surface at least 30 minutes a day, most days of the week (minimum 5) if not contraindicated. It is important to teach the patient and caregiver the proper use of NTG. NTG may be used prophylactically before an emotionally stressful situation, sexual intercourse, or physical exertion (e.g., climbing a long flight of stairs).

Chronic Stable Angina Collaborative Care

Angiotensin-converting enzyme inhibitors β-adrenergic blockers Calcium channel blockers Sodium current inhibitor Ranolazine (Ranexa) *Teacher Comment* Patients with chronic stable angina who are considered high risk for a cardiac event (e.g., ejection fraction [EF] 40% or less, history of diabetes) should take an ACE inhibitor (e.g., captopril [Capoten]) indefinitely. ACE inhibitors are also used for lower risk patients (e.g., patients with mildly reduced EF). These drugs result in vasodilation and reduced blood volume. Most importantly, they can prevent or reverse ventricular remodeling (see page 744). For patients who are intolerant of ACE inhibitors, angiotensin II receptor blockers (e.g., losartan [Cozaar]) are used. It is recommended that patients with left ventricular dysfunction, elevated BP, or who have had an MI start and continue β-adrenergic blockers indefinitely. These drugs decrease myocardial contractility, HR, SVR, and BP, all of which reduce the myocardial oxygen demand. β-adrenergic blockers have many side effects and can be poorly tolerated. Side effects may include bradycardia, hypotension, wheezing, and GI complaints. Many patients also complain of weight gain, depression, and sexual dysfunction. Patients with asthma should avoid β-adrenergic blockers. They are used cautiously in patients with diabetes as they mask signs of hypoglycemia. β-adrenergic blockers should not be discontinued abruptly without medical supervision. This may precipitate an increase in the frequency and intensity of angina attacks. If β-adrenergic blockers are contraindicated, are poorly tolerated, or do not control anginal symptoms, calcium channel blockers are used. These drugs are also used to manage Prinzmetal's angina. The three primary effects of calcium channel blockers are (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, and (3) coronary vasodilation. Most of these agents have sustained-release versions for longer action with the hope of increased patient adherence and stable blood levels of the drug. Ranolazine (Ranexa), a sodium current inhibitor, is used to treat chronic angina in those patients who have not achieved adequate response with other antianginals. Because ranolazine prolongs the Q-T interval, patients with a long Q-T interval or taking Q-T-prolonging drugs (e.g., fluoxetine [Prozac]) should not use it. Common side effects include dizziness, nausea, constipation, and generalized weakness.

Nursing ManagementAcute Coronary Syndrome

Coronary revascularization: CABG ICU for first 24-36 hours Pulmonary artery catheter Intraarterial line Pleural/mediastinal chest tubes Continuous ECG ET tube with mechanical ventilation Epicardial pacing wires Urinary catheter NG tube *Teacher Comment* For patients having CABG surgery, care is provided in the intensive care unit for the first 24 to 36 hours. Ongoing and intensive monitoring of the patient's hemodynamic status is critical. The patient will have numerous invasive lines for monitoring cardiac status and other vital organs. These include: A pulmonary artery catheter for measuring CO and other hemodynamic parameters An intraarterial line for continuous BP monitoring Pleural and mediastinal chest tubes for chest drainage Continuous ECG monitoring to detect dysrhythmias An endotracheal tube connected to mechanical ventilation Epicardial pacing wires for emergency pacing of the heart A urinary catheter to monitor urine output A nasogastric tube for gastric decompression Most patients will be extubated within 6 hours and transferred to a step-down unit within 24 hours for continued monitoring of cardiac status.

Nursing Management Chronic Stable Angina and ACS

Coronary revascularization: PCI Monitor for recurrent angina Frequent VS, including cardiac rhythm Monitor catheter insertion site for bleeding Neurovascular assessment Bed rest per institutional policy *Teacher comment* Patients with ACS may undergo coronary revascularization with PCI or CABG surgery. The major nursing responsibilities for the care of the patient following PCI involve: Monitoring for signs of recurrent angina Frequent assessment of vital signs, including HR and rhythm Evaluation of the catheter insertion site for signs of bleeding Neurovascular assessment of the involved extremity Maintenance of bed rest per institution policy

Collaborative CareAcute Coronary Syndrome

Coronary surgical revascularization -Failed medical management -Presence of left main coronary artery or three-vessel disease -Not a candidate for PCI (e.g., lesions are long or difficult to access) -Failed PCI with ongoing chest pain -History of diabetes mellitus -When long-term benefits of CABG are superior to those of PCI *Teacher Comment* Coronary revascularization with CABG surgery is recommended for patients who (1) fail medical management, (2) have left main coronary artery or three-vessel disease, (3) are not candidates for PCI (e.g., lesions are long or difficult to access), (4) have failed PCI and continue to have chest pain, (5) have diabetes mellitus, or (6) when the long-term benefits of CABG are superior to those of PCI.

Collaborative CareAcute Coronary Syndrome

Coronary surgical revascularization 1. Coronary artery bypass graft (CABG) surgery -Requires sternotomy and cardiopulmonary bypass (CPB) -Uses arteries and veins for grafts 2. Minimally invasive direct coronary artery bypass (MIDCAB) -Alternative to traditional CABG *Teacher Comment* CABG surgery consists of the placement of conduits to transport blood between the aorta, or other major arteries, and the myocardium distal to the blocked coronary artery (or arteries). CABG surgery requires a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). The procedure may involve one or more grafts using the internal mammary artery, saphenous vein, radial artery, gastroepiploic artery, and/or inferior epigastric artery. Minimally invasive direct coronary artery bypass (MIDCAB) is a technique that offers patients with limited disease an approach to surgical treatment that does not involve a sternotomy and CPB. The technique requires several small incisions between the ribs. A thoracoscope is used to dissect the IMA. The heart is slowed using a β-adrenergic blocker (e.g., esmolol [Brevibloc]) or stopped temporarily with adenosine. A mechanical stabilizer immobilizes the operative site.

Collaborative CareAcute Coronary Syndrome

Coronary surgical revascularization Off-pump coronary artery bypass Sternotomy but no CPB Robot-assisted surgery Transmyocardial laser revascularization Indirect revascularization High-energy laser creates channels in heart to allow blood flow *Teacher Comment* The off-pump coronary artery bypass (OPCAB) procedure uses full or partial sternotomy to access all coronary vessels. OPCAB is performed on a beating heart using mechanical stabilizers and without CPB. It is usually reserved for patients with limited disease but who are at high risk for traditional surgery secondary to multiple co-morbidities. Robot-assisted cardiothoracic surgery incorporates the use of a robot in performing CABG or mitral valve replacement. The benefits of robotic surgery include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time. Transmyocardial laser revascularization (TMR) is an indirect revascularization procedure. It is used for patients with advanced CAD who are not candidates for traditional CABG surgery and who have persistent angina after maximum medical therapy. The procedure involves the use of a high-energy laser to create channels in the heart to allow blood flow to ischemic areas. The procedure is performed during cardiac catheterization as a percutaneous TMR or during surgery using a left anterior thoracotomy incision as an adjunct to CABG.

Chronic Stable Angina Collaborative Care

Diagnostic studies Chest x-ray Laboratory studies 12-lead ECG Calcium-score screening heart scan Echocardiogram Exercise stress test Pharmacologic nuclear imaging *Teacher Comment* When a patient has a history of CAD or CAD is suspected, a variety of studies are completed. After a detailed health history and physical examination, a chest x-ray is done to look for cardiac enlargement, aortic calcifications, and pulmonary congestion. A 12-lead ECG is obtained and compared with a previous tracing when possible. Certain laboratory tests (e.g., lipid profile) and diagnostic studies (e.g., echocardiogram) are done to confirm CAD and identify specific risk factors for CAD. A calcium-score screening heart scan locates calcium deposits in atherosclerotic plaque in the coronary arteries. Additional testing (e.g., stress testing) is needed to know the impact of the lesion on coronary blood flow. Exercise stress testing and pharmacologic nuclear imaging are also useful.

Complications of Myocardial Infarction

Dressler syndrome -Pericarditis with effusion and fever that develops 4 to 6 weeks after MI -Pericardial (chest) pain -Pericardial friction rub -Pericardial effusion -Arthralgia -Treated with short-term corticosteroids *Teacher Comment* Dressler syndrome is pericarditis with effusion and fever that develops 4 to 6 weeks after MI. It is thought to be caused by an antigen-antibody reaction to the necrotic myocardium. The patient experiences pericardial pain, fever, a friction rub, pericardial effusion, and arthralgia. Laboratory findings include an elevated white blood cell count and sedimentation rate. Short-term corticosteroids are used to treat this condition.

Complications of Myocardial Infarction

Dysrhythmias Most common complication Present in 80% of MI patients Can be caused by ischemia, electrolyte imbalances, or SNS stimulation Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock *Teacher Comment* The most common complication after an MI is dysrhythmias, which are present in 80% to 90% of patients. Dysrhythmias are the most common cause of death in patients in the prehospital period. Any condition that affects the myocardial cell's sensitivity to nerve impulses (e.g., ischemia, electrolyte imbalances, SNS stimulation) can cause dysrhythmias. The intrinsic rhythm of the heart is disrupted. This can cause tachycardia, bradycardia, or an irregular HR, all of which adversely affect the ischemic myocardium. Life-threatening dysrhythmias occur most often with anterior wall infarction, HF, or shock. Complete heart block develops when key portions of the conduction system are destroyed. Ventricular fibrillation, a common cause of sudden cardiac death (SCD), is a lethal dysrhythmia. It most often occurs within the first 4 hours after the onset of pain. Premature ventricular contractions may precede ventricular tachycardia and fibrillation. Life-threatening ventricular dysrhythmias must be treated immediately.

Nursing ManagementAcute Coronary Syndrome

Evaluation Stable vital signs Relief of pain Decreased anxiety Realistic program of activity Effective management of therapeutic regimen *Teacher Comment* The overall expected outcomes are that the patient with ACS: Maintains stable signs of effective cardiac output Reports relief of pain Reports decreased anxiety and increased sense of self-control Achieves a realistic program of activity that balances physical activity with energy-conserving activities Describes the disease process, measures to reduce risk factors, and rehabilitation activities necessary to manage the therapeutic regimen

Myocardial Infarction From Occlusion

MIs are usually described based on the location of damage (e.g., anterior, inferior, lateral, septal, or posterior wall infarction). Most involve some portion of the left ventricle. The location of the infarction correlates with the involved coronary circulation. For example, the right coronary artery provides blood supply to the inferior wall. Blockage of the right coronary artery will result in an inferior wall MI. Anterior wall infarctions result from blockages in the left anterior descending artery, as shown in this figure. Blockages in the left circumflex artery usually cause lateral and/or posterior wall MIs. Damage can occur in more than one location, especially if more than one coronary artery is involved (e.g., anterolateral MI, anteroseptal MI). The degree of preexisting collateral circulation also influences the severity of infarction. An individual with a long history of CAD will develop collateral circulation to provide the area surrounding the infarction site with a blood supply. This is one reason why a younger person may have a more serious first MI than an older person with the same degree of blockage.

Collaborative CareAcute Coronary Syndrome

Initial interventions -12-lead ECG -Semi-fowler's position -Oxygen -IV access -Nitroglycerin (SL) and ASA (chewable) -Morphine *Teacher Comment* It is extremely important to rapidly diagnose and treat a patient with ACS to preserve cardiac muscle. Obtain a 12-lead ECG and start continuous ECG monitoring. Position the patient in an upright position unless contraindicated and initiate oxygen by nasal cannula to keep oxygen saturation above 93%. Establish an IV route to provide an access for emergency drug therapy. Give sublingual NTG and aspirin (chewable) if not given before arrival at the ED. Morphine sulfate is given for pain unrelieved by NTG.

Clinical Manifestations of CAD Angina

Lack of oxygen and glucose leads to anaerobic metabolism Lactic acid irritates nerve fibers → pain in cardiac nerves Referred pain from transmission to the upper thoracic posterior nerve roots *Teacher Comment* Myocardial cells are deprived of oxygen and glucose needed for aerobic metabolism and contractility. Anaerobic metabolism begins and lactic acid accumulates. Lactic acid irritates myocardial nerve fibers and transmits a pain message to the cardiac nerves and upper thoracic posterior nerve roots. This accounts for referred cardiac pain to the shoulders, neck, lower jaw, and arms.

Collaborative and Nursing Management: CAD

Lipid-lowering drug therapy Fibric acid derivatives (Lopid) Decrease triglycerides and increase HDL GI side effects Bile acid sequestrants Increase conversion of cholesterol to bile acids GI side effects; bind with other drugs Ezetimibe (Zetia) Decrease absorption of dietary and biliary cholesterol *Teacher Comment* The fibric acid derivatives work by aiding the removal of VLDLs and increasing the production of apolipoproteins A-I and A-II. They are the most effective drugs for lowering triglycerides and increasing HDL levels. They have no effect on LDLs. Although most patients tolerate the drugs well, complaints may include GI irritability. Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol. The primary effect is a decrease in total cholesterol and LDLs. Administration of these drugs can be associated with complaints related to taste and a variety of upper and lower GI symptoms. These include belching, heartburn, nausea, abdominal pain, and constipation. The bile-acid sequestrants interfere with absorption of many other drugs (e.g., warfarin, thiazides, thyroid hormones, β-adrenergic blockers). Separating the time of administration of these drugs from other drugs decreases this adverse effect. Drugs that Decrease Cholesterol Absorption Ezetimibe (Zetia) selectively inhibits the absorption of dietary and biliary cholesterol across the intestinal wall. It serves as an adjunct to dietary changes, especially in patients with primary hypercholesterolemia. Drug therapy for hyperlipidemia often continues for a lifetime. Concurrent diet modification is essential to minimize the need for drug therapy. The patient must fully understand the rationale and goals of treatment, as well as the safety and side effects of lipid-lowering drug therapy.

collaberative and nursing management for CAD patients

Lipid-lowering drug therapy If diet and exercise ineffective Statins Inhibit cholesterol synthesis, decrease LDL, increase HDL Monitor for liver damage and myopathy Niacin Lowers LDL and triglyceride by inhibiting synthesis Increases HDL Flushing, pruritus, GI side effects, orthostatic hypotension *Teacher Comment* The person with a serum cholesterol level >200 mg/dL is at risk for CAD and should be treated. Treatment usually begins with dietary caloric restriction (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity. Serum lipid levels are reassessed after 6 weeks of diet therapy. If they remain elevated, additional dietary options and drug therapy may be considered. There are several classifications of drugs that are used to decrease serum lipids. Drugs that Restrict Lipoprotein Production The statin drugs are the most widely used lipid-lowering drugs. These drugs inhibit the synthesis of cholesterol in the liver. An unexplained result of the inhibition of cholesterol synthesis is an increase in hepatic LDL receptors. Consequently, the liver is able to remove more LDLs from the blood. In addition, statins produce a small increase in HDLs and lower CRP levels. Serious adverse effects of these drugs are rare and include liver damage and myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle). Liver enzymes (e.g., aspartate aminotransferase, alanine aminotransferase) are initially monitored and rechecked with any increase in dosage. Niacin (Niaspan), a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs. Unfortunately, side effects of this drug are common and may include severe flushing, pruritus, gastrointestinal (GI) symptoms, and orthostatic hypotension.

Collaborative and Nursing Management: CAD

Manage high-risk persons by controlling modifiable risk factors Encourage lifestyle changes Education Clarify personal values Set realistic goals *Teacher Comment* Management of High-Risk Persons Recommend preventive measures for all persons at risk for CAD. Risk factors such as age, gender, ethnicity, and genetic inheritance cannot be modified. However, the person with any of these risk factors can still reduce the risk of CAD by controlling the additive effects of modifiable risk factors. For example, a young man with a family history of heart disease can decrease the risk of CAD by maintaining an ideal body weight, getting adequate physical exercise, reducing intake of saturated fats, and avoiding tobacco use. People who have modifiable risk factors should be encouraged to make lifestyle changes to reduce their risk of CAD. You can play a major role in teaching health-promoting behaviors. For highly motivated persons, knowing how to reduce this risk may be the information that they need to get started. For persons who are less motivated to take charge of their health, the idea of reducing risk factors may be so remote that they are unable to perceive a threat of CAD. Few people desire to make lifestyle changes, especially in the absence of symptoms. You should first assist these patients in clarifying personal values. Then, by explaining the risk factors and having them identify their vulnerability to various risks, you may help them recognize their susceptibility to CAD. This may help patients set realistic goals and allow them to choose which risk factor(s) to change first. Some persons are reluctant to change until they begin to manifest overt symptoms or actually suffer an MI. Others, having suffered an MI, may find the idea of changing lifelong habits still unacceptable. You must be able to identify such choices and respect them.

Risk Factors for CAD-Modifiable

Modifiable risk factors Elevated serum lipids Cholesterol >200 mg/dL (5.2 mmol/L) Triglycerides >150 mg/dL (3.7 mmol/L) High-density lipoproteins (HDL) Low-density lipoproteins (LDL) Treatment according to guidelines based on 10-year risk score *Teacher Comment* Modifiable risk factors include elevated serum lipids, elevated blood pressure, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and elevated homocysteine level. Elevated Serum Lipids An elevated serum lipid level is one of the four most firmly established risk factors for CAD. The risk of CAD is associated with a serum cholesterol level of more than 200 mg/dL (5.2 mmol/L) or a fasting triglyceride level of more than 150 mg/dL (3.7 mmol/L). For lipids to be used and transported by the body, they must become soluble in blood by combining with proteins. Lipids combine with proteins to form lipoproteins. Lipoproteins are vehicles for fat mobilization and transport, and vary in composition. They are classified as high-density lipoproteins (HDLs), LDLs, and very-low-density lipoproteins (VLDLs). HDLs carry lipids away from arteries and to the liver for metabolism. Therefore, high serum HDL levels are desirable and lower the risk of CAD. In general, HDL levels are higher in women, decrease with age, and are low in persons with CAD. Physical activity, moderate alcohol consumption, and estrogen administration increase HDL levels. LDLs contain more cholesterol than any of the lipoproteins and have an attraction for arterial walls. Elevated LDL levels correlate most closely with an increased incidence of atherosclerosis and CAD. Therefore, low serum LDL levels are desirable. Guidelines for treating elevated LDL cholesterol are based on a person's 10-year risk for having a nonfatal MI or dying from a coronary event and his or her LDL levels. The following information generates a risk score: (1) age, (2) gender, (3) use of tobacco, (4) systolic BP, (5) use of BP drugs, (6) total cholesterol, and (7) HDL cholesterol level. A 10-year risk calculator is available at http://hin.nhlbi.nih.gov/atpiii/calculator.asp?usertype=prof. In general, individuals with no or only one risk factor are considered at low risk for the development of CAD, and the LDL goal is <160 mg/dL (4.14 mmol/L). Those at very high risk have CAD and multiple risk factors. The LDL goal for this group is <70 mg/dL (1.8 mmol/L).

Risk Factors for CAD-Modifiable

Modifiable risk factors Hypertension >140/90 mm Hg or >130/80 mm Hg if diabetes or CKD Begin lifestyle changes for prehypertension Treat stage 1 or 2 hypertension with drugs *Teacher Comment* Hypertension The second major risk factor in CAD is hypertension, which is defined as a BP >140/90 mm Hg or >130/80 mm Hg if the patient has diabetes or chronic kidney disease. Hypertension increases the risk of death from CAD 10-fold in all persons. The stress of an elevated BP increases the rate of atherosclerotic development. This relates to the shearing stress that causes endothelial injury. Therapeutic lifestyle changes should begin in people with prehypertension (BP of 120 to 139 mm Hg/80 to 89 mm Hg). Those with stage 1 or 2 hypertension often require more than one drug to reach therapeutic goals.

Risk factors for CAD

Modifiable risk factors Physical inactivity Obesity Diabetes Metabolic syndrome *Teacher Comment* Physical Inactivity Physical inactivity is the fourth major modifiable risk factor. Physical inactivity implies a lack of adequate physical exercise on a regular basis. An example of health-promoting regular physical activity is brisk walking (3 to 4 miles per hour) for at least 30 minutes 5 or more times a week. Physically active people have increased HDL levels. Exercise improves thrombolytic activity, thus reducing the risk of clot formation. Exercise may also encourage the development of collateral circulation in the heart. Obesity The mortality rate from CAD is statistically higher in obese persons. Obesity is defined as a body mass index (BMI) of >30 kg/m2 and a waist circumference ≥40 inches for men and ≥35 inches for women. The increased risk for CAD is proportional to the degree of obesity. There is also evidence that people who tend to store fat in the abdomen (an "apple" figure) rather than in the hips and buttocks (a "pear" figure) have a higher incidence of CAD. As obesity increases, the heart grows and uses more oxygen. In addition, there is an increase in insulin resistance in obese individuals. Diabetes The incidence of CAD is 2 to 4 times greater among persons who have diabetes, even those with well-controlled blood glucose levels, than the general population. The patient with diabetes manifests CAD not only more frequently but also at an earlier age. The person with diabetes has an increased tendency toward endothelial dysfunction. This may account for the development of fatty streaks seen in these patients. Diabetic patients also have alterations in lipid metabolism and tend to have high cholesterol and triglyceride levels. Management of diabetes should include lifestyle changes and drug therapy to achieve a hemoglobin A1c (Hb A1c) level <7%. Metabolic Syndrome Metabolic syndrome refers to a cluster of risk factors for CAD whose underlying pathophysiology may be related to insulin resistance. These risk factors include obesity as defined by increased waist circumference, hypertension, abnormal serum lipids, and an elevated fasting blood glucose.

Risk Factors for CAD

Modifiable risk factors Tobacco use Increased catecholamine release ↑ LDL, ↓ HDL, ↑oxygen radicals ↑ Carbon monoxide Second-hand smoke *Teacher Comment* Tobacco Use A third major risk factor in CAD is tobacco use. The risk of developing CAD is two to six times higher in those who smoke tobacco or use smokeless tobacco than in those who do not. Further, tobacco smoking decreases estrogen levels, placing premenopausal women at greater risk for CAD. Risk is proportional to the number of cigarettes smoked. Changing to lower nicotine or filtered cigarettes does not affect risk. Nicotine in tobacco smoke causes catecholamine (i.e., epinephrine, norepinephrine) release. These neurohormones cause an increased heart rate (HR), peripheral vasoconstriction, and increased BP. These changes increase the cardiac workload. Tobacco smoke is also related to an increase in LDL level, a decrease in HDL level, and release of toxic oxygen radicals. All of these add to vessel inflammation and thrombosis. Carbon monoxide, a byproduct of combustion found in tobacco smoke, affects the oxygen-carrying capacity of hemoglobin by reducing the sites available for oxygen transport. Thus the effects of an increased cardiac workload, combined with the oxygen-depleting effect of carbon monoxide, significantly decrease the oxygen available to the myocardium. There is also some indication that carbon monoxide is a chemical irritant, and causes injury to the endothelium. The benefits of smoking cessation are dramatic and almost immediate. CAD mortality rates drop to those of nonsmokers within 12 months. However, nicotine is highly addictive and often calls for intensive intervention to assist people to quit. Chronic exposure to environmental tobacco (secondhand) smoke also increases the risk of CAD. People who live in the same household as the patient should be encouraged to stop smoking. This reinforces the individual's effort and decreases the risk of ongoing exposure to environmental smoke. Pipe and cigar smokers, who often do not inhale, have an increased risk of CAD similar to those exposed to environmental tobacco smoke.

Gerontologic ConsiderationsCAD

Necessary to modify guidelines for physical activity Longer warm-up Longer periods of low-level activity Longer rest periods Avoid extremes of temperature 30 minutes most days minimum Most likely to change when hospitalized or symptomatic *Teacher Comment* Similarly, you should encourage the older patient to consider a planned program of physical activity. Activity performance, endurance, and ability to tolerate stress are improved in the older adult with physical training. Positive psychologic benefits can be derived from physical activity and can include increased self-esteem and emotional well-being and improved body image. For the older adult who is obese, making modest dietary changes and slowly increasing physical activity (e.g., walking) will result in more positive benefits than aiming for a significant weight loss. When planning a physical activity program for the older adult, recommend the following: (1) longer warm-up periods, (2) longer periods of low-level activity, or (3) longer rest periods between sessions. Heat intolerance in the older adult results from a decreased ability to sweat efficiently. Teach the patient to avoid physical activity in extremes of temperature and to maintain a moderate pace. The older adult should exercise a minimum of 30 minutes on most days of the week as able. Encouraging the older patient to adopt a healthy lifestyle may increase the quality of life and reduce the risk of CAD and fatal cardiac events. The older adult faces many of the same challenges when it comes to making lifestyle changes. There are two points in time when the older adult is more likely to consider change: (1) when hospitalized and (2) when symptoms (e.g., chest pain) are the result of CAD and not normal aging. First, assess the older adult for readiness to change and then help the patient to select the lifestyle changes most likely to produce the greatest reduction in risk for CAD.

Clinical Manifestations of ACS Unstable Angina

New in onset Occurs at rest Worsening pattern Increase in frequency Unpredictable Medical emergency Symptoms in women may be more vague *Teacher Comment* Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening pattern. The patient with chronic stable angina may develop UA, or UA may be the first clinical sign of CAD. The patient with previously diagnosed chronic stable angina will describe a significant change in the pattern of angina. It will occur with increasing frequency and is easily provoked by minimal or no exertion, during sleep, or even at rest. Unlike chronic stable angina, UA is unpredictable and is an emergency. Despite national efforts to increase awareness, women's symptoms continue to go unrecognized as heart related. These include fatigue, shortness of breath, indigestion, and anxiety. Fatigue is the most prominent symptom. However, all these symptoms can relate to many different diseases and syndromes. It is because of these reasons that women often present with UA before CAD is diagnosed.

Sudden Cardiac Death (SCD)

No warning signs or symptoms if no MI Prodromal symptoms if associated with MI Chest pain, palpitations, dyspnea Death usually within 1 hour of onset of acute symptoms *Teacher Comment* Persons who experience SCD because of CAD fall into two groups: (1) those who did not have an acute MI and (2) those who did have an acute MI. The first group accounts for the majority of cases of SCD. In this instance, victims usually have no warning signs or symptoms. Patients who survive are at risk for another SCD event due to the continued electrical instability of the myocardium that caused the initial event to occur. The second, smaller group of patients includes those who have had an MI and have suffered SCD. In these cases, patients usually have prodromal symptoms, such as chest pain, palpitations, and dyspnea. Death usually occurs within 1 hour of the onset of acute symptoms.

Chronic Stable AnginaTypes of Angina

Nocturnal angina Occurs only at night but not necessarily during sleep Angina decubitus Chest pain that occurs only while lying down Relieved by standing or sitting *Teacher Comment* Nocturnal angina occurs only at night but not necessarily when the person is in the recumbent position or during sleep. Angina decubitus is chest pain that occurs only while the person is lying down and is usually relieved by standing or sitting.

Risk factors for CAD

Nonmodifiable risk factors Age Gender Ethnicity Family history Genetic predisposition *Teacher Comment* Risk factors are characteristics or conditions that are associated with a high incidence of a disease. Many risk factors have been associated with CAD. They are categorized as nonmodifiable and modifiable Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetic inheritance. The incidence of CAD and MI is highest among white, middle-aged men. After age 65, the incidence in men and women equalizes, although cardiovascular disease causes more deaths in women than men. On average, women with CAD are older than men who have CAD, and are more likely to have co-morbidities (e.g., hypertension, diabetes). Most women have atypical symptoms of angina rather than MI when presenting with their initial cardiac event. African Americans have an earlier onset and more severe CAD than there CAD counterparts. Additionally, CAD incidence and mortality rates are greater in African American women than their white counterparts. Family history is a risk factor for CAD and MI. Most times, patients with angina or MI can name a parent or sibling who has died of CAD. The genetic basis of CAD/MI is complex and poorly understood. It is estimated that the genetic contribution to CAD/MI is as high as 40% to 60%. This proportion relates mainly to genes that control known risk factors (e.g., lipid metabolism).

Nursing ManagementChronic Stable Angina and ACS

Nursing assessment: objective data Anxious, fearful, restless, distressed Cool, clammy, pale skin Tachycardia or bradycardia Pulsus alternans (alternating weak and strong heartbeats) Pulse deficit Dysrhythmias S3, S4, ↑ or ↓ BP, murmur

Nursing ManagementChronic Stable Angina and ACS

Nursing assessment: subjective data Family history Indigestion/heartburn; nausea/vomiting Urinary urgency or frequency Straining at stool Palpitations, dyspnea, dizziness, weakness Chest pain Stress, depression, anger, anxiety *Teacher Comment* Also obtain the following important health information related to pertinent functional health patterns: Health perception-health management: Family history of heart disease; sedentary lifestyle; tobacco use; exposure to environmental smoke Nutritional-metabolic: Indigestion, heartburn, nausea, belching, vomiting Elimination: Urinary urgency or frequency, straining at stool Activity-exercise: Palpitations, dyspnea, dizziness, weakness Cognitive-perceptual: Substernal chest pain or pressure (squeezing, constricting, aching, sharp, tingling), possible radiation to jaw, neck, shoulders, back, or arms (see Table 34-7) Coping-stress tolerance: Stressful lifestyle, depression; anger, anxiety; feeling of impending doom

Nursing Management Chronic Stable Angina and ACS

Nursing diagnoses Decreased cardiac output Acute pain Anxiety Activity intolerance Ineffective self-health management *Teacher comment* Decreased cardiac output related to altered contractility and altered heart rate and rhythm as evidenced by decrease in BP, elevation in HR, dyspnea, dysrhythmias, diminished pulses, peripheral edema, and/or pulmonary edema Acute pain related to an imbalance between myocardial oxygen supply and demand as evidenced by patient's report of severe chest pain and tightness with radiation of pain to the neck and arms, elevated cardiac markers, ECG changes Anxiety related to perceived or actual threat of death, pain, and/or possible lifestyle changes as evidenced by restlessness, agitation, and verbalization of concern over lifestyle changes and prognosis as evidenced by patient's statement of "What if I die ... everyone relies on me." Activity intolerance related to general weakness secondary to decreased cardiac output and poor lung and tissue perfusion as evidenced by patient's report of fatigue with minimal activity, inability to care for self without dyspnea, and increased heart rate Ineffective self-health management related to lack of knowledge of disease process, risk factor reduction, rehabilitation, home activities, and drugs as evidenced by frequent questioning about illness, management, and care after discharge

Collaborative CareAcute Coronary Syndrome

Nutritional therapy -Initially NPO -Progress to Low salt Low saturated fat Low cholesterol *Teacher Comment* Initially, patients may be NPO (nothing by mouth), except for sips of water, until stable (e.g., pain free, nausea resolved). You advance the diet as tolerated to a low-salt, low-saturated fat, and low-cholesterol diet

Collaborative and Nursing Management: CAD

Nutritional therapy ↓ Saturated fats and cholesterol ↑ Complex carbohydrates and fiber ↓ Red meat, egg yolks, whole milk ↑Omega-3 fatty acids *Teacher Comment* The National Heart, Lung, and Blood Institute recommends therapeutic lifestyle changes for all people to reduce the risk of CAD by lowering LDL cholesterol. These recommendations emphasize a decrease in saturated fat and cholesterol and an increase in complex carbohydrates (e.g., whole grains, fruit, vegetables) and fiber. Red meat, egg yolks, and whole milk products are major sources of saturated fat and cholesterol and should be reduced or eliminated from diets. If the serum triglyceride level is elevated, the guidelines recommend reducing or eliminating alcohol intake and simple sugars. Omega-3 fatty acids reduce the risks associated with CAD when eaten regularly. For individuals without CAD, the AHA recommends eating fatty fish twice a week because fatty fish such as salmon and tuna contain two types of omega-3 fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Patients with CAD are encouraged to take EPA and DHA supplements with their diet. The AHA also recommends eating tofu and other forms of soybean, canola, walnut, and flaxseed because these products contain alpha-linolenic acid, which becomes omega-3 fatty acid in the body.

Collaborative CareAcute Coronary Syndrome

Ongoing monitoring -Treat dysrhythmias -Frequent vital sign monitoring -Bed rest/limited activity for 12-24 hours UA or NSTEMI -Aspirin, heparin, and glycoprotein inhibitor -Coronary angiography with PCI once stable *Teacher Comment* The patient will usually receive ongoing care in a critical care unit or telemetry unit, where continuous ECG monitoring is available. Dysrhythmias are treated according to established protocols. Monitor vital signs, including pulse oximetry, frequently during the first few hours after admission and closely thereafter. Maintain bed rest and limitation of activity for 12 to 24 hours, with a gradual increase in activity unless contraindicated. For patients with UA or NSTEMI with negative cardiac markers and ongoing angina: A combination of aspirin, heparin (UH or LMWH), and a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]) is recommended. Coronary angiography with possible PCI is considered once the patient is stabilized and angina is controlled, or if angina returns or increases in severity.

Clinical Manifestations of ACS Myocardial Infarction

Pain Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration Heaviness, pressure, tightness, burning, constriction, crushing Substernal, retrosternal, epigastric More common in AM Atypical in women, elderly No pain if cardiac neuropathy (diabetes) *Teacher Comment* Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. Persistent and unlike any other pain, it is usually described as a heaviness, pressure, tightness, burning, constriction, or crushing. Common locations are substernal, retrosternal, or epigastric areas. When epigastric pain is present, the patient may relate it to indigestion and take antacids without relief. The pain may radiate to the neck, lower jaw, and arms or to the back It may occur while the patient is active or at rest, asleep, or awake. However, it commonly occurs in the early morning hours. It usually lasts for 20 minutes or longer and is more severe than usual anginal pain. Not everyone has classic symptoms. Some patients may not experience pain but may have "discomfort," weakness, or shortness of breath. Although women and men have more similarities in their symptoms of an acute MI than differences, some women may experience atypical discomfort, shortness of breath, or fatigue. An older patient may experience a change in mental status (e.g., confusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia. Patients with diabetes may experience silent (asymptomatic) MIs due to cardiac neuropathy and have atypical symptoms (e.g., dyspnea).

Collaborative and Nursing Management: CAD

Prevention and early treatment Identification of people at high risk Health history, including family history Presence of cardiovascular symptoms Environmental patterns: diet, activity Psychosocial history Values and beliefs about health and illness *Teacher Comment* The appropriate management of risk factors in CAD may prevent, modify, or slow the progression of the disease. In the United States during the past 26 years, there has been a gradual and persistent decline in cardiovascular-related deaths. The decline relates to the efforts of people to become generally healthier, as well as advances in pharmacology and technology to treat CAD. Prevention and early treatment of heart disease must involve a multifaceted approach and needs to be ongoing throughout the life span. Identification of High-Risk Persons Clinical manifestations of CAD will not be apparent in the early stages of the disease. Therefore, it is extremely important to identify people at risk for CAD. Risk screening involves obtaining a thorough health history. Question the patient about a family history of heart disease in parents and siblings. Note the presence of any cardiovascular symptoms. Assess environmental factors, such as eating habits, type of diet, and level of exercise to elicit lifestyle patterns. Include a psychosocial history to determine tobacco use, alcohol ingestion, recent stressful events (e.g., loss of a spouse), and the presence of any negative psychologic states (e.g., anxiety, depression, anger). The place of work and the type of work provides important information on the kind of activity performed, exposure to pollutants or noxious chemicals, and the degree of stress associated with work. Identify the patient's attitudes and beliefs about health and illness. This information can give some indication of how disease and lifestyle changes may affect the patient and can reveal possible misconceptions about heart disease.

Chronic Stable AnginaTypes of Angina

Prinzmetal's (variant) angina Occurs at rest usually in response to spasm of major coronary artery Seen in patients with a history of migraine headaches and Raynaud's phenomenon Spasm may occur in the absence of CAD

Internal Mammary Artery and Saphenous Vein Grafts

The internal mammary artery (IMA) is the most common artery used for bypass graft. It is left attached to its origin (the subclavian artery) but then dissected from the chest wall. Next, it is anastomosed (connected with sutures) to the coronary artery distal to the blockage. The long-term patency rate for IMA grafts is greater than 90% after 10 years. Saphenous veins are also used for bypass grafts. The surgeon removes the saphenous vein from one or both legs endoscopically. Sections are attached to the ascending aorta and then to a coronary artery distal to the blockage. The use of antiplatelet therapy and statins after surgery improves vein graft patency. Patency rates of these grafts are 50% to 60% at 10 years.

Collaborative CareAcute Coronary Syndrome

Thrombolytic therapy -When PCI not available -Stops infarction process by dissolving thrombus -Within 6 hours of onset of symptoms -Ideally within first hour -Given IV -Patient selection critical *Teacher Comment* Thrombolytic therapy offers the advantages of availability and rapid administration in facilities that do not have an interventional cardiac catheterization laboratory or one is too far away to transfer the patient safely. Treatment of MI with thrombolytic therapy aims to stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium. Thrombolytic therapy is given as soon as possible, ideally within the first hour after onset of symptoms and preferably within the first 6 hours after the onset of symptoms. Mortality is reduced by 25% if reperfusion occurs within 6 hours. All thrombolytics are given IV. Because all thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a postoperative site). Therefore patient selection is important because minor or major bleeding can be a complication of therapy. Inclusion criteria for thrombolytic therapy include (1) chest pain typical of acute MI 6 hours or less in duration, (2) 12-lead ECG findings consistent with acute MI, and (3) no absolute contraindications. Although patients with chest pain greater than 6 hours in duration and ECG changes supporting MI may be considered for thrombolytic therapy, benefits of this therapy are inconsistent.

Collaborative CareAcute Coronary Syndrome

Thrombolytic therapy Draw blood and start 2-3 IV sites Complete invasive procedures prior Administer according to protocol Monitor closely for signs of bleeding Assess for signs of reperfusion Return of ST segment to baseline best marker IV heparin to prevent reocclusion *Teacher Comment* Each hospital has a protocol for giving thrombolytic therapy. However, there are several common factors. Draw blood to obtain baseline laboratory values and start two or three lines for IV therapy. All other invasive procedures are done before the thrombolytic agent is given to reduce the possibility of bleeding in the patient. Depending on the drug selected, therapy is administered in one IV bolus or over a period of time (30 to 90 minutes). Evaluate heart rhythm, vital signs, and pulse oximetry, and assess the heart and lungs frequently to evaluate the patient's response to therapy. Regularly assess for changes in neurologic status as this may indicate a cerebral bleed. When reperfusion occurs (i.e., the coronary artery that was blocked is opened and blood flow is restored to the myocardium), several clinical markers may occur. The most reliable marker is the return of the ST segment to baseline on the ECG. Other markers include a resolution of chest pain, and an early, rapid rise of the cardiac markers within 3 hours of therapy and peaking within 12 hours. These levels increase as the necrotic myocardial cells release proteins into the circulation after perfusion is restored to the area. The presence of reperfusion dysrhythmias (e.g., accelerated idioventricular rhythm) is a less reliable marker of reperfusion. These dysrhythmias are generally self-limiting and do not require aggressive treatment. A major concern with thrombolytic therapy is reocclusion of the artery. The site of the thrombus is unstable, and another clot may form or spasm of the artery may occur. Because of this possibility, IV heparin therapy is initiated.

Collaborative CareAcute Coronary Syndrome

Thrombolytic therapy When PCI not available Stops infarction process by dissolving thrombus Within 6 hours of onset of symptoms Ideally within first hour Given IV Patient selection critical *Teacher Comment* Thrombolytic therapy offers the advantages of availability and rapid administration in facilities that do not have an interventional cardiac catheterization laboratory or one is too far away to transfer the patient safely. Treatment of MI with thrombolytic therapy aims to stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium. Thrombolytic therapy is given as soon as possible, ideally within the first hour after onset of symptoms and preferably within the first 6 hours after the onset of symptoms. Mortality is reduced by 25% if reperfusion occurs within 6 hours. All thrombolytics are given IV. Because all thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a postoperative site). Therefore patient selection is important because minor or major bleeding can be a complication of therapy. Inclusion criteria for thrombolytic therapy include (1) chest pain typical of acute MI 6 hours or less in duration, (2) 12-lead ECG findings consistent with acute MI, and (3) no absolute contraindications. Although patients with chest pain greater than 6 hours in duration and ECG changes supporting MI may be considered for thrombolytic therapy, benefits of this therapy are inconsistent.

Sudden Cardiac Death (SCD)

Unexpected death from cardiac causes Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow Most commonly caused by ventricular dysrhythmias Structural heart disease Conduction disturbances *Teacher Comment* Sudden cardiac death (SCD) is unexpected death resulting from a variety of cardiac causes. In SCD, there is a sudden disruption in cardiac function, producing an abrupt loss of CO and cerebral blood flow. The affected person may or may not have a known history of heart disease. SCD is often the first sign of illness for 25% of those who die of heart disease. Acute ventricular dysrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) cause the majority of cases of SCD. Structural heart disease accounts for 10% of the cases of SCD. Patients in this group include those with left ventricular hypertrophy, myocarditis, and hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a risk factor for SCD, especially in young, athletic people. Approximately 10% to 12% of cases of SCD among people less than age 45 occur in the absence of structural heart disease. These involve disturbances in the conduction system (e.g., prolonged QT syndrome, Wolff-Parkinson-White syndrome).

Acute Coronary Syndrome Etiology and Pathophysiology

deterioration of once stable plaque -> Rupture -> platelet aggregation -> Thrombus Result Partial occlusion of coronary artery: UA or NSTEMI Total occlusion of coronary artery: STEMI *Teacher Comment* ACS is associated with deterioration of a once stable atherosclerotic plaque. The once stable plaque ruptures, exposing the intima to blood and stimulating platelet aggregation and local vasoconstriction with thrombus formation. This unstable lesion may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI). What causes a coronary plaque to suddenly become unstable is not well understood, but systemic inflammation is thought to play a role. Patients with suspected ACS require immediate hospitalization.