Epidemiology of Coronary Artery Disease, Valve Disease, and Need for Heart Surgery



Epidemiology of Coronary Artery Disease, Valve Disease, and Need for Heart Surgery







Heart disease is one of the most common causes of death in the world. Symptoms may begin gradually, but for many people severe symptoms strike suddenly. Nurses need to be aware of the symptoms of and treatments available for heart disease to manage patients with both slowly progressive disease and disease with sudden onset.






Objectives


In this chapter, you will learn:



1.  The symptoms of coronary artery disease and acute coronary syndrome


2.  When someone with coronary artery disease would need coronary artery bypass graft surgery


3.  When disease of the cardiac valves would require surgery


4.  Key points in caring for patients with congenital heart disease


CORONARY ARTERY DISEASE


Coronary artery disease (CAD) is one of the leading deadly diseases in the world. It is estimated that each year in the United States alone, over 780,000 people experience acute coronary syndrome (ACS). About 70% of these will experience non–ST segment elevation ACS (Amsterdam et al.). In 2009, 386,324 Americans died of CAD, which was approximately 1 out of every 6 deaths in the United States (Go et al., 2013). If recognized and treated early, long-term damage from myocardial infarction (MI) and ischemia can be prevented or made less severe.


Symptoms of CAD


CAD is the buildup of plaque consisting of fatty material and inflammatory cells inside the wall of one or more coronary arteries (Figure 1.1). As the disease progresses and these plaques grow in size, they begin to weaken the wall of the artery and grow into the lumen of the artery. Calcium may be deposited in large plaques, hardening them, and they often become large enough to impede the flow of blood. Most people who have CAD are unaware that they have this disease until they experience symptoms. Symptoms of CAD are related to a lack of blood flow to the heart muscle (ischemia) and are called anginal symptoms or angina. Traditionally, chest pain and chest pressure were considered the primary anginal symptoms, often accompanied by pain radiating to the jaw or arm, nausea, diaphoresis, or shortness of breath. It is now recognized that many people, especially women, diabetics, and the elderly, may experience atypical symptoms. These are symptoms that generally occur without chest pain or pressure and may include unexplained weakness or fatigue, nausea, indigestion, dizziness, or back pain (Jacobson, Marzlin, & Webner, 2007).



FIGURE 1.1    Atherosclerosis.


Stable angina refers to symptoms that occur with physical exertion or stress and subside with rest. Typically, these stable symptoms are caused by the slow buildup of atherosclerotic plaque in the walls of the coronary arteries. As the arteries narrow, they are not able to supply sufficient blood to meet the increased demand during exercise or other stresses that increase the heart rate. Once the heart rate slows (usually during rest), oxygen demand decreases and symptoms subside. Symptoms that do not subside with rest may signal a more deadly progression of CAD: ACS.


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Ischemia from CAD is caused by a mismatch between oxygen supply and oxygen demand. The resulting myocardial ischemia may cause a variety of symptoms.






ACUTE CORONARY SYNDROME


CAD often begins years before ACS strikes. An inflammatory process causes plaque to build up in the coronary arteries. People with certain risk factors, as noted in Table 1.1, are more likely to have plaque buildup, especially if their diagnoses are severe or if more than one risk factors is present. As the buildup process evolves, the plaque may become unstable and prone to rupture. If a coronary artery plaque ruptures, the inflammatory cells in the plaque cause platelets to be activated, triggering the clotting cascade, which causes formation of a clot in the artery. The severity of the episode and amount of damage to the heart muscle depend on the extent of the clot.


ACS is a spectrum of diseases, including unstable angina (USA), non–ST segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI). USA is caused by a thrombus in the coronary artery that resolves spontaneously through the body’s own thrombolytic system. If at some point a clot forms and the body is unable to break it apart, USA progresses to either NSTEMI or STEMI.


 





TABLE 1.1  Risk Factors for CAD















Nonmodifiable risk factors:


  Family history—premature CAD (younger than 55 in men and younger than 65 in women) in a first-degree relative (mother, father, sibling)


  Older age (over 65)


  Gender—men are at higher risk than women until women reach menopause


Modifiable risk factors:


  Cigarette smoking


  Dyslipidemia


  Hypertension


  Diabetes mellitus


  Abdominal obesity


  Lack of physical activity


  Low daily fruit and vegetable consumption


  Overconsumption of alcohol


  Psychosocial risk factors—stress, depression, anxiety, anger, and hostility






CAD, coronary artery disease.


Source: Jacobson et al. (2007).


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ACS is a sudden and life-threatening event caused by rupture of an unstable atherosclerotic plaque. The resulting blood clot in the artery causes myocardial ischemia or infarction, or both, depending on the amount of blood flow that is occluded.






Unstable Angina


USA occurs when a clot occludes or partially occludes a coronary artery, then is broken down by the body’s fibrinolytic system, restoring blood flow. Anginal symptoms occur, and then subside. Symptoms may occur at rest or with minimal exertion and typically last more than 20 minutes. These anginal symptoms tend to recur, often with increasing severity and frequency.


Non–ST Segment Elevation Myocardial Infarction


NSTEMI refers to a clot that has partially occluded a coronary artery causing anginal symptoms. Some blood continues to reach the myocardium, but it provides an insufficient supply of oxygen and nutrients to the cells. This results in ischemia, which may be detected by changes such as ST depression or T-wave inversion on a 12-lead electrocardiogram (ECG), by an increase in cardiac enzymes, or both.


ST Segment Elevation Myocardial Infarction


If the clot completely blocks the flow of blood to the myocardium, the result is STEMI. The blockage of blood flow causes ischemia at first, then necrosis (death of myocardial cells). As cardiac muscle cells die, they no longer conduct electrical current, which results in elevation of ST segments on a 12-lead ECG. (See Table 1.2 for information on how to determine which artery is blocked by looking at the 12-lead ECG.) The death of myocardial cells also causes enzymes, normally found inside these muscle cells, to be released into the bloodstream. This leads to an increase in cardiac enzymes in the bloodstream. (See Table 1.3 for onset time of commonly measured cardiac enzymes.)


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Patients with STEMI need to have the occluded artery opened emergently to save the heart muscle. Thrombolytics should be administered within 30 minutes of the patient’s arrival (door to drug time). If angioplasty and stenting will be used, the artery must be opened within 90 minutes (door to balloon time).






Treatment of Acute Coronary Syndrome


Treatment of ACS involves administering medications, evaluating the extent of the disease, and restoring blood flow to ischemic areas of the heart.


 





TABLE 1.2  Coronary Arteries and Corresponding ECG Leads




























Coronary Artery


ECG Lead


Location of Myocardial Infarction


RCA


II, III, aVF


Inferior


LAD


V1, V2
V1, V2, V3, V4


Septal
Anterior


LCx


I, aVL, V5, V6


Lateral






LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery.


 





TABLE 1.3  Onset, Peak, and Duration of Serum Cardiac Enzyme Levels After an Ischemic Episode







Medications Used in Acute Coronary Syndrome


As described above, patients with ACS have a thrombus partially or completely occluding a coronary artery. Medications are aimed at preventing further growth of the clot, shrinking the clot, and minimizing damage done by ischemia. A patient presenting with symptoms of ACS should immediately be given an aspirin and placed on oxygen, as ordered by a physician. Aspirin is an antiplatelet medication that slows the growth of the thrombus. Administering oxygen increases the supply of oxygen available in the blood for ischemic tissues. Nitroglycerin administered sublingually is quickly absorbed into the bloodstream. The vasodilatory effect of nitroglycerin allows increased blood flow to ischemic areas. If chest pain or other anginal symptoms are not relieved with three doses of nitroglycerin, morphine should be given, per physician’s order. Morphine simultaneously calms the patient, decreasing oxygen demand, and dilates coronary arteries to increase blood supply.


CLINICAL ALERT! Caution should be used when administering nitroglycerin and morphine. Neither should be given if the systolic blood pressure is below 90 mmHg. Nitroglycerin should not be given if the patient has taken medications for erectile dysfunction, as the combination may cause dangerously low blood pressure.


Evaluating Coronary Artery Disease


When patients are experiencing ACS, it is important to determine the extent of CAD. Most patients who present with ACS need to undergo angiography to definitively determine how much CAD is present and decide on treatment. (See Chapter 2 for a description of coronary angiography.)


Revascularization


Patients who have a thrombus completely occluding a coronary artery (STEMI) need immediate treatment to open the blocked artery. This can be done using medications or in the cardiac cath lab with percutaneous coronary intervention (PCI).


Thrombolytics may be used to open an occluded artery. Tenecteplase (TNK) is a commonly used thrombolytic for STEMI and must be ordered by a physician. Patients need to be screened prior to administration of thrombolytics due to high risk of bleeding. Thrombolytics are contraindicated in patients who have recently had a stroke or major trauma, who have severe uncontrolled hypertension, or have suspected aortic dissection. Extreme caution should be used when administering a thrombolytic to a patient who has had recent gastrointestinal bleeding or recent major surgery, or one who is taking anticoagulants. If a patient experiencing STEMI is to receive a thrombolytic, the medication should be given as soon as possible. The goal for of thrombolytic treatment in patients with STEMI is to administer within 30 minutes of presentation to an emergency department.


It is the responsibility of the physician ordering the thrombolytic to screen patients for contraindications. However, nurses need to be aware of the contraindications and notify the physician if any are present; the nurse may have information not available to the physician. Nurses should not administer a medication that is contraindicated.


Hospitals with a cardiac cath lab and the ability to perform cardiac interventions should use PCI, when possible, to open the artery of a patient experiencing STEMI. PCI includes thrombectomy (directly removing the clot using a catheter in the coronary artery), angioplasty (inflating a balloon at the end of a catheter in the area of occlusion in the coronary artery), and stenting (placing a small tube of metal in the coronary artery to hold the artery open). The goal for patients with STEMI should be to have the artery open within 90 minutes of presentation to an emergency department.


Need for Surgery


Patients with a small number of focal coronary artery lesions and those that are easily reached using PCI are usually treated using angioplasty and stenting. A catheter is threaded through an artery (usually femoral or radial) and pushed forward until it is advanced into the diseased coronary artery. A balloon at the end of the catheter is inflated at the site of the coronary artery plaque and essentially smashes the plaque against the walls of the artery to increase the size of the lumen of the artery. This catheter is removed and a second catheter is advanced to the same place. At the end of this catheter is a small tube of metal called a stent (Figure 1.2). As the balloon at the end of the catheter is inflated, the stent expands to the size of the artery and holds the artery open. The stent remains in place and the catheter is removed.


Many patients who have multiple lesions or diffuse disease (narrowing of a significant portion of the coronary arteries) need surgical repair with coronary artery bypass grafting (CABG). Also, patients who have valve disease or other structural heart disease that requires surgical repair typically have CABG at the time of valve repair rather than undergoing PCI for CAD (see Table 1.4). An interventional cardiologist and cardiac surgeon should review the films and clinical presentation of patients with complicated disease or anatomy to determine, with the input of the patient, the best strategy for revascularization (Hillis et al., 2011).



FIGURE 1.2    Percutaneous coronary intervention—stent placement.


Nurses play an important role in reinforcing the rationale for PCI versus cardiac surgery. An understanding of the rationale for each helps nurses as they educate patients and prepare them for surgery or other treatments.


FAST FACTS in a NUTSHELL


Jul 2, 2017 | Posted by in NURSING | Comments Off on Epidemiology of Coronary Artery Disease, Valve Disease, and Need for Heart Surgery

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