Promoting Cessation of Tobacco Use

Cigarette smoking contributes to the development and severity of CAD in the following three ways:
• The inhalation of smoke increases the blood carbon monoxide level. Hemoglobin, the oxygen-carrying
component of blood, combines more readily with carbon monoxide than with oxygen. A decreased
amount of available oxygen may decrease the heart’s ability to pump.
• The nicotinic acid in tobacco triggers the release of catecholamines, which raise the heart rate and
blood pressure. Nicotinic acid can also cause the coronary arteries to constrict. Smokers have an
increased risk of CAD and sudden cardiac death (Porth & Matfin, 2009). The increase in
catecholamines
may be a factor in sudden cardiac death.
• Use of tobacco adversely affects the vascular endothelium, resulting in increased platelet adhesion and
leading to a higher probability of thrombus formation. A person at increased risk for heart disease is
encouraged to stop tobacco use through any means possible: educational programs, counseling,
consistent motivation and Some people have found complementary therapies (eg, acupuncture, guided
imagery, hypnosis) to be helpful. People who stop smoking reduce their risk of heart disease within the
first year, and the risk continues to decline as long as they refrain from smoking (Lichtenstein, et al.,
2006).
Use of medications such as the nicotine patch (Nico-Derm CQ, Habitrol) or the antidepressant bupropion
(Zyban) may assist with stopping use of tobacco (Fraker, Fihn, Gibbons, et al., 2007). Products
containing nicotine have some of the same effects as smoking: catecholamine release (increasing heart
rate and blood pressure) and increased platelet adhesion. These medications should be used for a short
time and at the lowest effective doses.
Exposure to other smokers’ smoke (passive or secondhand smoke) is believed to cause heart disease in
nonsmokers (Office of the U.S. Surgeon General, 2006). Oral contraceptive use by women who smoke is
inadvisable because these medications significantly increase the risk for CAD and sudden cardiac death.
Managing Hypertension
Hypertension is defined as blood pressure measurements that repeatedly exceed 140/90 mm Hg. The
risk of cardiovascular disease increases as blood pressure increases, and people with a blood pressure
greater than 120/80 mm Hg are considered prehypertensive and at risk (Rosendorff, Black, Cannon, et
al., 2007). Long-standing elevated blood pressure may result in increased stiffness of the vessel walls,
leading to vessel injury and a resulting inflammatory response within the intima. Inflammatory mediators
then lead to the release of growth-promoting factors that cause vessel hypertrophy and
hyperresponsiveness. These changes result in acceleration and aggravation of atherosclerosis.
Hypertension also increases the work of the left ventricle, which must pump harder to eject blood into the
arteries. Over time, the increased workload causes the heart to enlarge and thicken (ie, hypertrophy) and
may eventually lead to heart failure. Early detection of high blood pressure and adherence to a

therapeutic regimen can prevent the serious consequences associated with untreated elevated blood
pressure. Hypertension is discussed in detail in Chapter 32.
Controlling Diabetes Mellitus
Diabetes mellitus is known to accelerate the development of heart disease, and for 65% to 75% of
patients with diabetes, cardiovascular disease is identified as the cause of death (Zipes, Libby, Bonow, et
al., 2005). Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell
function, which can lead to thrombus formation. It has been suggested that these metabolic alterations
impair endothelial cell–dependent vasodilation and smooth muscle function, promoting the development
of atherosclerosis. Treatment with insulin (eg, Humulin, Novolin) and metformin (Glucophage) and other
therapeutic interventions that lower plasma glucose levels can lead to improved endothelial function and
patient outcomes. Diabetes is discussed in detail in Chapter 41.
Angina Pectoris
episodes or paroxysms of pain or pressure in the anterior chest.
insufficient coronary blood flow, decreased oxygen supply, increased myocardial demand for oxygen
effect on activities of daily living
Pathophysiology
caused by atherosclerotic disease… obstruction of at least one major coronary artery…increasing
myocardial oxygen demand, menyebabkan terjadi masalah ketika: Physical exertion, Exposure to cold,
Eating a heavy meal, Stress or any emotion-provoking situation,
Assessment and Diagnostic Findings
The diagnosis of angina begins with the patient’s history related to the clinical manifestations of ischemia.
A 12-lead electrocardiogram (ECG) may show changes indicative of ischemia such as T-wave inversion.
Laboratory studies are performed; these may include CRP and cardiac biomarker values to rule out an
ACS (refer to later discussion on ACS). The patient may undergo an exercise or pharmacologic stress
test in which the heart is monitored by an ECG, echocardiogram, or both. The patient may also be
referred for a nuclear scan or invasive procedure (eg, cardiac catheterization, coronary angiography).
Medical Management
The objectives of the medical management of angina are to decrease the oxygen demand of the
myocardium and to increase the oxygen supply. Medically, these objectives are met through
pharmacologic therapy and control of risk factors. Alternatively, reperfusion procedures may be used to
restore the blood supply to the myocardium. These include PCI procedures (eg, percutaneous
transluminal coronary angioplasty [PTCA], intracoronary stents, and atherectomy) and CABG.
Pharmacologic Therapy
Table 28-3 summarizes drug therapy.
Nitroglycerin
Nitrates are an important treatment for angina pectoris. A vasoactive agent, nitroglycerin is administered
to reduce myocardial oxygen consumption, which decreases ischemia and relieves pain. Nitroglycerin
dilates primarily the veins and, in higher doses, the arteries. Dilation of the veins causes venous pooling
of blood throughout the body. As a result, less blood returns to the heart, and filling pressure (preload) is
reduced. If the patient is hypovolemic (does not have adequate circulating blood volume), the decrease in
filling pressure can cause a significant decrease in cardiac output and blood pressure. Nitrates in higher
doses also relax the systemic arteriolar bed, lowering blood pressure and decreasing afterload.
These effects decrease myocardial oxygen requirements and increase oxygen supply, bringing about a
more favorable balance between supply and demand. Nitroglycerin may be given by several routes:
sublingual tablet or spray, oral capsule, topical agent, and intravenous (IV) administration. Sublingual
nitroglycerin is generally placed under the tongue or in the cheek (buccal pouch) and ideally alleviates the
pain of ischemia within 3 minutes.
Chart 28-3 provides more information on self-administration of sublingual nitroglycerin. Oral preparations
and topical patches are used to provide sustained effects. The patches are often applied in the morning
and removed at bedtime. This regimen allows for a nitrate-free period to prevent the development of
tolerance. A continuous or intermittent IV infusion of nitroglycerin may be administered to the
hospitalized
patient with recurring signs and symptoms of ischemia or after a revascularization procedure. The dose of
nitroglycerin administered is based on the patient’s symptoms while avoiding side effects such as
hypotension. It usually is not administered if the systolic blood pressure is 90 mm Hg or less. Generally,

after the patient is symptom-free, the nitroglycerin may be switched to an oral or topical preparation
within
24 hours.
Beta-Adrenergic Blocking Agents
Beta-blockers such as metoprolol (Lopressor, Toprol) and atenolol (Tenormin) reduce myocardial oxygen
consumption by blocking beta-adrenergic sympathetic stimulation to the heart. The result is a reduction in
heart rate, slowed conduction of impulses through the conduction system, decreased blood pressure, and
reduced myocardial contractility (force of contraction) to balance the myocardial oxygen needs
(demands) and the amount of oxygen available (supply). This helps control chest pain and delays the
onset of ischemia during work or exercise. Beta-blockers reduce the incidence of recurrent angina,
infarction, and cardiac mortality. The dose can be titrated to achieve a resting heart rate of 50 to 60 bpm
(beats per minute).
Cardiac side effects and possible contraindications include hypotension, bradycardia, advanced
atrioventricular block, and acute heart failure. If a beta-blocker is given intravenously for an acute cardiac
event, the ECG, blood pressure, and heart rate are monitored closely after the medication has been
administered. Side effects include depression, fatigue, decreased libido, and masking of symptoms of
hypoglycemia.
Patients taking beta-blockers are cautioned not to stop taking them abruptly, because angina may worsen
and MI may develop. Beta-blocker therapy should be decreased gradually over several days before being
discontinued. Patients with diabetes who take beta-blockers are instructed to monitor their blood glucose
levels often and to observe for signs and symptoms of hypoglycemia. Beta-blockers that are not
cardioselective also affect the beta-adrenergic receptors in the bronchioles, causing bronchoconstriction,
and therefore are contraindicated in patients with significant chronic pulmonary disorders, such as
asthma.