ANGINA PECTORIS

Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply. The severity of angina is based on the precipitating activity and its effect on the activities of daily living

Pathophysiology

Angina is usually caused by atherosclerotic disease. Almost invariably, angina is associated with a significant obstruction of a major coronary artery.
Several factors are associated with typical anginal pain: Physical exertion, which can precipitate an attack by increasing myocardial oxygen demand Exposure to cold, which can cause vasoconstriction and an elevated blood pressure, with increased oxygen demand

 Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle (In a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain.) Stress or any emotion-provoking situation, causing the release of adrenaline and increasing blood pressure, which may accelerate the heart rate and increase the myocardial workload peripheral vascular disease, arthritis, degenerative disk disease, physical disability, foot problems) that limit the patients ability to exercise.

Types of Angina

Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest Unstable angina (also called preinfarction angina or crescendo angina): symptoms occur more frequently and last longer than stable angina. The threshold for pain is lower, and pain may occur at rest. Intractable or refractory angina: severe incapacitating chest pain Variant angina (also called Prinzmetals angina): pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no symptoms

Clinical Manifestations

Ischemia of the heart muscle may produce pain or other symptoms, varying in severity from a feeling of indigestion to a choking or heavy sensation in the upper chest that ranges from discomfort to agonizing pain accompanied by severe apprehension and a feeling of impending death. The pain is often felt deep in the chest behind the upper or middle third of the sternum (retrosternal area). Typically, the pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm. The patient often feels tightnessor a heavy, choking, or strangling sensation that has a viselike, insistent quality. The patient with diabetes mellitus may not have severe pain with angina because the neuropathy that accompanies diabetes can interfere with neuroreceptors, dulling the patients perception of pain.

A feeling of weakness or numbness in the arms, wrists, and hands may accompany the pain, as may shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting. These symptoms may also appear alone and still represent myocardial ischemia. When these symptoms appear alone, they are called angina-like symptoms. Anxiety may accompany angina. An important characteristic of angina is that it abates or subsides with rest or nitroglycerin.

Assessment and Diagnostic Findings

The diagnosis of angina is often made by evaluating the clinical manifestations of ischemia and the patients history. A 12-lead ECG and blood laboratory values help in making the diagnosis. The patient may undergo an exercise or pharmacologic stress test in which the heart is monitored by ECG, echocardiogram, or both. The patient may also be referred for an echocardiogram,nuclear scan, or invasive procedures (cardiac catheterization and coronary artery angiography).

CAD is believed to result from inflammation of the arterial endothelium. C-reactive protein (CRP) is a marker for inflammation of vascular endothelium. High blood levels of CRP have been associated with increased coronary artery calcification and risk of an acute cardiovascular event (eg, MI) in seemingly healthy individuals There is interest in using CRP blood levels as an additional risk factor for cardiovascular disease in clinical use and research, but the clinical value of CRP levels has not been fully established. The ability of CRP to predict cardiovascular disease when adjusted for other risk factors, how CRP levels can guide patient management, and if patient outcomes improve when using CRP levels must be established before CRP levels are used routinely for patient care

An elevated blood level of homocysteine, an amino acid, has also been proposed as an independent risk factor for cardiovascular disease. However, studies have not supported the relationship between mild to moderate elevations of homocysteine and atherosclerosis No study has yet shown that reducing homocysteine levels reduces the risk of CAD.

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. Revascularization procedures to restore the blood supply to the myocardium include percutaneous coronary interventional (PCI) procedures (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary stents, and atherectomy), CABG, and percutaneous transluminal myocardial revascularization(PTMR).

Nitroglycerin. Nitrates remain the mainstay for treatment of angina pectoris. A vasoactive agent, nitroglycerin (Nitrostat, Nitrol, Nitrobid IV) is administered to reduce myocardial oxygen consumption, which decreases ischemia and relieves pain. Nitroglycerin dilates primarily the veins and, in higher doses, also dilates the arteries. It helps to increase coronary blood flow bypreventing vasospasm and increasing perfusion through the collateral vessels. 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 and lower blood pressure (decreased afterload). Nitrates may increase blood flow to diseased coronary arteries and through collateral coronary arteries, arteries that have been underused until the body recognizes poorly perfused areas. 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, topical agent, and intravenous administration. Sublingual nitroglycerin is generally placed under the tongue or in the cheek (buccal pouch) and alleviates the pain of ischemia within 3 minutes. Topical nitroglycerin is also fast acting and is a convenient way to administer the medication. Both routes are suitable for patients who self-administer the medication.

A continuous or intermittent intravenous infusion of nitroglycerin may be administered to the hospitalized patient with recurring signs and symptoms of ischemia or after a revascularization procedure. The amount of nitroglycerin administered is based on the patients symptoms while avoiding side effects such as hypotension. It usually is not given if the systolic blood pressure is 90 mm Hg or less. Generally, after the patient is symptom free, the nitroglycerin may be switched to a topical preparation within 24 hours.

Beta-Adrenergic Blocking Agents. Beta-blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol), and atenolol (Tenormin) appear to reduce myocardial oxygen consumption by blocking the beta-adrenergic sympathetic stimulation to the heart. The result is a reduction in heart rate, slowed conduction of an impulse through the heart, decreased blood pressure, and reduced myocardial contractility (force of contraction) that establishes a more favorable balance between myocardial oxygen needs (demands) and the amount of oxygen available (supply). This helps to 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 beats per minute.

Cardiac side effects and possible contraindications include hypotension, bradycardia, advanced atrioventricular block, and decompensated 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. Because some beta-blockers also affect the beta-adrenergic receptors in the bronchioles, causing bronchoconstriction, they are contraindicated in patients with significant pulmonary constrictive diseases, such as asthma. Other side effects include worsening of hyperlipidemia, 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 needs tobe decreased gradually over several days before discontinuing it. Patients with diabetes who take beta-blockers are instructed to assess their blood glucose levels more often and to observe for signs and symptoms of hypoglycemia.

Calcium Channel Blocking Agents. Calcium channel blockers (calcium ion antagonists) have different effects. Some decrease sinoatrial node automaticity and atrioventricular node conduction, resulting in a slower heart rate and a decrease in the strength of the heart muscle contraction (negative inotropic effect). These effects decrease the workload of the heart. Calcium channel blockers also relax the blood vessels, causing a decrease in blood pressure and an increase in coronary artery perfusion. Calcium channel blockers increase myocardial oxygen supply by dilating the smooth muscle wall of the coronary arterioles; they decrease myocardial oxygen demand by reducing systemic arterial pressure and the workload of the left ventricle.

The calcium channel blockers most commonly used are amlodipine (Norvasc), verapamil (Calan, Isoptin, Verelan), and diltiazem (Cardizem, Dilacor, Tiazac). They may be used by patients who cannot take beta-blockers, who develop significant side effects from beta-blockers or nitrates, or who still have pain despite betablocker and nitroglycerin therapy. Calcium channel blockers are used to prevent and treat vasospasm, which commonly occurs after an invasive interventional procedure. Use of short-acting nifedipine (Procardia) was found to be poorly tolerated and to increase the risk of MI in patients with hypertension and the risk of death in patients with acute coronary syndrome

First-generation calcium channel blockers should be avoided or used with great caution in people with heart failure, because they decrease myocardial contractility. Amlodipine (Norvasc) and felodipine (Plendil) are the calcium channel blockers of choice for patients with heart failure. Hypotension may occur after the intravenous administration of any of the calcium channel blockers. Other side effects that may occur include atrioventricular blocks, bradycardia, constipation, and gastric distress.

Antiplatelet and Anticoagulant Medications. Antiplatelet medications are administered to prevent platelet aggregation, which impedes blood flow. Aspirin.
Aspirin prevents platelet activation and reduces the incidence of MI and death in patients with CAD. A 160- to 325-mg dose of aspirin should be given to the patient with angina as soon as the diagnosis is made (eg, in the emergency room or physicians office) and then continued with 81 to 325 mg daily. Although it may be one of the most important medications in the treatment of CAD, aspirin may be overlooked because of its low cost and common use. Patients should be advised to continue aspirin even if concurrently taking nonsteroidal antiinflammatory drugs (NSAIDs) or other analgesics. Because aspirin may cause gastrointestinal upset and bleeding, treatment of Helicobacter pylori and the use of H2-blockers (eg, cimetidine [Tagamet], famotidine [Mylanta AR, Pepcid], ranitidine [Zantac]) or misoprostol (Cytotec) should be considered to allow continued aspirin therapy.

Clopidogrel and Ticlopidine

Clopidogrel (Plavix) or ticlopidine(Ticlid) is given to patients who are allergic to aspirin or given in addition to aspirin in patients at high risk for MI. Unlike aspirin, these medications take a few days to achieve their antiplatelet effect. They also cause gastrointestinal upset, including nausea, vomiting, and diarrhea, and they decrease the neutrophil level. Unfractionated heparin prevents the formation of new blood clots. Use of heparin alone in treating patients with unstable angina reduces the occurrence of MI. If the patients signs and symptoms indicate a significant risk for a cardiac event, the patient is hospitalized and may be given an intravenous bolus of heparin and started on a continuous infusion or given an intravenous bolus every 4 to 6 hours. The amount of heparin administered is based on the results of the activated partial thromboplastin time (aPTT). Heparin therapy is usually considered therapeutic when the a PTT is 1.5 to 2 times the normal aPTT value.

Heparin

A subcutaneous injection of low-molecular-weight heparin (LMWH; enoxaparin [Lovenox] or dalteparin [Fragmin]) may be used instead of intravenous unfractionated heparin to treat patients with unstable angina or nonST-segment elevation MIs. LMWH provides more effective and stable anticoagulation, potentially reducing the risk of rebound ischemic events, and it eliminates the need to monitor aPTT results. LMWH may be beneficial before and during PCIs and for Stsegment elevation MIs. Because unfractionated heparin and LMWH increase the risk of bleeding, the patient is monitored for signs and symptoms of external and internal bleeding, such as low blood pressure, an increased heart rate, and a decrease in serum hemoglobin and hematocrit values. The patient receiving heparin is placed on bleeding precautions, which include: Applying pressure to the site of any needle puncture for a longer time than usual Avoiding intramuscular injections Avoiding tissue injury and bruising from trauma or use of constrictive devices (eg, continuous use of an automatic blood pressure cuff) Decrease in platelet count or skin lesions at heparin injection sites may indicate heparin-induced thrombocytopenia (HIT), an antibody-mediated reaction to heparin that may result in thrombosis Patients who have received heparin within the past 3 months and those who have been receiving unfractionated heparin for 5 to 15 days are at high risk for HIT.

GPIIb/IIIa Agents.

GPIIb/IIIa Agents. Intravenous GPIIb/IIIa agents (abciximab [ReoPro], tirofiban [Aggrastat], eptifibatide [Integrelin]) are indicated for hospitalized patients with unstable angina and as adjuncttherapy for PCI. These agents prevent platelet aggregation by blocking the GPIIb/IIIa receptors on the platelet, preventing adhesion of fibrinogen and other factors that crosslink platelets to each other and thereby allow platelets to form a thrombus (clot). As with heparin, bleeding is the major side effect, and bleeding precautions should be initiated.

Oxygen Administration

Oxygen therapy is usually initiated at the onset of chest pain in an attempt to increase the amount of oxygen delivered to the myocardium and to decrease pain. Oxygen inhaled directly increases the amount of oxygen in the blood. The therapeutic effectiveness of oxygen is determined by observing the rate and rhythm of respirations. Blood oxygen saturation is monitored by pulse oximetry; the normal oxygen saturation (SpO2) level is greater than 93%. Studies are being conducted to assess the use of oxygen in patients without respiratory distress and its effect on outcome.

ALTERNATIVE THERAPIES

Researchers have reported significant improvement in the exercise endurance of patients with angina who were treated with acupuncture as well as with an intravenous infusion of a combination of ginseng (Panax quinquefolium), astragalus (Astragalus membranaceus), and angelica Coenzyme Q10 was advocated for preventing the occurrence and progression of heart failure However, there have not been large, randomized, placebocontrolled studies that identify the direct beneficial effect from these therapies.

TREATING ANGINA

If the patient reports pain (or the individuals equivalent to pain), the nurse takes immediate action. When a patient experiences angina, the nurse should direct the patient to stop all activities and sit or rest in bed in a semiFowler position to reduce the oxygen requirements of the ischemic myocardium. The nurse assesses the patients angina, asking questions to determine whether the angina is the same as the patient typically experiences. A difference may indicate a worsening of the disease or a different cause. The nurse then continues to assess the patient, measuring vital signs and observing for signs of respiratory distress. If the patient is in thehospital, a 12-lead ECG is usually obtained and scrutinized for ST-segment and T-wave changes. If the patient has been placed oncardiac monitoring with continuous ST-segment monitoring, the ST segment is assessed for changes. Nitroglycerin is administered sublingually, and the patients response is assessed (relief of chest pain and effect on blood pressure and heart rate). If the chest pain is unchanged or is lessened but still present, nitroglycerin administration is repeated up to three doses.

Each time, blood pressure, heart rate, and the ST segment (if the patient is on a monitor with ST segment monitoring capability) are assessed. The nurse administers oxygen therapy if the patients respiratory rate is increased or the oxygen saturation level is decreased. Although there is no documentation of its effect on outcome, oxygen is usually administered at 2 L/min by nasal cannula, even without evidence of respiratory distress. If the pain is significant and continues after these interventions, the patient is usually transferred to a higher-acuity nursing unit.

REDUCING ANXIETY

Patients with angina often fear loss of their roles within society and the family. They may also be fearful that the pain may lead to an MI or death. Exploring the implications that the diagnosis has for the patient and providing information about the illness, its treatment, and methods of preventing its progression are important nursing interventions. Various stress reduction methods should be explored with the patient. For example, music therapy, in which patients are given the opportunity to listen to selected music through headphones for a predetermined duration, has been shown to reduce anxiety in patients who are in a coronary care unit and may serve as an adjunct to therapeutic communication Addressing the spiritual needs of the patient and family may also assist in allaying anxieties and fears.

PREVENTING PAIN

The nurse reviews the assessment findings, identifies the level of activity that causes the patients pain, and plans the patients activities accordingly. If the patient has pain frequently or with minimal activity, the nurse alternates the patients activities with rest periods. Balance of activity and rest is an important aspect of the educational plan for the patient and family.

MYOCARDIAL INFARCTION

Pathophysiology

MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed. Like unstable angina, MI is usually caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus. Because unstable angina and acute MI are considered to be the same process but different points along a continuum, the term acute coronary syndrome (ACS) may be used for these diagnoses. Other causes of an MI include vasospasm (sudden constriction or narrowing) of a coronary artery; decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure); and increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine). In each case, a profound imbalance exists between myocardial oxygen supply and demand.

Coronary occlusion, heart attack, and MI are terms used synonymously, but the preferred term is MI. The area of infarction takes time to develop. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and over time, the lack of oxygen results in infarction, or the death of cells. The expression time is muscle reflects the urgency of appropriate treatment to improve patient outcomes. Various descriptions are used to further identify an MI: the location of the injury to the left ventricular wall (anterior, inferior, posterior, or lateral wall) or to the right ventricle and the point in time within the process of infarction (acute, evolving, or old). The ECG usually identifies the location, and the ECG and patient history identify the timing. Regardless of the location of the infarction of cardiac muscle, the goal of medical therapy is to prevent or minimize myocardial tissue death and to prevent complications.

Clinical Manifestations

Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with an MI . One study showed that 2% of patients who eventually were diagnosed with an acute MI were incorrectly discharged and sent home from the emergency department. Most of these patients presented with atypical symptoms such as shortness of breath; they also tended to be female, younger than 55 years of age, of a minority group, and have normal ECGs. The Framingham Heart Study revealed that 50% of the men and 63% of the women who died suddenly of cardiovascular disease had no previous symptoms. Patients may also be anxious and restless. They may have cool, pale,and moist skin. Their heart rate and respiratory rate may be faster than normal. These signs and symptoms, which are caused by stimulation of the sympathetic nervous system, may be present only for a short time or may not be present, or only some of them may occur. In many cases, the signs and symptoms of MI cannot be distinguished from those of unstable angina.

Signs and Symptoms of an Acute Myocardial Infarction (MI) or Acute Coronary Syndrome (ACS)

Cardiovascular: Chest pain or discomfort, palpitations. Heart sounds may include S3, S4, and new onset of a murmur. Increased jugular venous distention may be seen if the MI has caused heart failure. Blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased contractility, impending cardiogenic shock, or medications. Pulse deficit may indicate atrial fibrillation. In addition to STsegment and T-wave changes, ECG may show tachycardia, bradycardia, and dysrhythmias.

Respiratory: Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion. Pulmonary edema may be present. Gastrointestinal: Nausea and vomiting. Genitourinary: Decreased urinary output may indicate cardiogenic shock. Skin: Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation from loss of contractility may indicate cardiogenic shock. Dependent edema may also be present due to poor contractility.

Neurologic: Anxiety, restlessness, light-headedness may indicate increased sympathetic stimulation or a decrease in contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock. Headache, visual disturbances, altered speech, altered motor function, and further changes in level of consciousness may indicate cerebral bleeding if patient is receiving thrombolytics. Psychological: Fear with feeling of impending doom, or patient may deny that anything is wrong.

Assessment and Diagnostic Findings

Diagnosis of MI is generally based on the presenting symptoms, the ECG, and laboratory test results (eg, serial serum enzyme values). The prognosis depends on the severity of coronary artery obstruction and the extent of myocardial damage. Physical examination is always conducted, but the examination alone is insufficient to confirm the diagnosis.

PATIENT HISTORY

The patient history has two parts: the description of the presenting symptom (eg, pain) and the history of previous illnesses and family health history, particularly of heart disease. Previous history should also include information about the patients risk factors for heart disease.

ELECTROCARDIOGRAM

The ECG provides information that assists in diagnosing acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the emergency department. By monitoring the ECG over time, the location, evolution, and resolution of an MI can be identified and monitored. The ECG changes that occur with an MI are seen in the leads that view the involved surface of the heart. The classic ECG changes are T-wave inversion, ST-segment elevation, and development of an abnormal Q wave . Because infarction evolves over time, the ECG also changes over time. The first ECG signs of an acute MI are from myocardial ischemia and injury. Myocardial injury causes the T wave to become enlarged and symmetric. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert.

The ischemic region may remain depolarized while adjacent areas of the myocardium return to the resting state. Myocardial injury also causes ST-segment changes. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line (area between the T wave and the next P wave is used as the reference for the isoelectric line) when measured 0.08 seconds after the end of the QRS. If the myocardial injury is on the endocardial surface, the ST segment is depressed 1 mm or more for at least 0.08 seconds. The ST-segment depression is usually horizontal or has a downward slope.

MI is classified as a Q-wave or non-Q-wave infarction. With Q-wave infarction, abnormal Q waves develop within 1 to 3 days because there is no depolarization current conducted from necrotic tissue .The lead system then views the flow of current from other parts of the heart. An abnormal Q wave is 0.04 seconds or longer, 25% of the R-wave depth (provided the R wave exceeds a depth of 5 mm), or one that did not exist before the event. An acute MI may cause a significant decrease in the height of the R wave. During an acute MI, injury and ischemic changes are also present. An abnormal Q wave may be present without ST-segment and T-wave changes, which indicates an old, not acute, MI. Patients with non-Q-wave MIs do not develop a Q wave on the ECG after the ST-segment and T-wave changes, but symptoms and cardiac enzyme analysis confirm the diagnosis of an MI.

During recovery from an MI, the ST segment often is the first to return to normal (1 to 6 weeks). The T wave becomes large and symmetric for 24 hours, and it then inverts within 1 to 3 days for 1 to 2 weeks. Q-wave alterations are usually permanent. An old Qwave MI is usually indicated by an abnormal Q wave or decreased height of the R wave without ST-segment and T-wave changes.