ANGINA PECTORIS Description

1. Angina is chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply. 2. Angina is caused by an imbalance between oxygen supply and demand. 3. Causes include obstruction of coronary blood flow because of atherosclerosis, coronary artery spasm, and conditions increasing myocardial oxygen consumption. 4. The goal of treatment is to provide relief of an acute attack, correct the imbalance between myocardial oxygen supply and demand, and prevent the progression of the disease ad further attacks to reduce the risk of MI. Patterns of angina 1. Stable angina

Stable angina also called exertional angina. Stable angina occurs with activities that involve exertion or emotional stress and is relieved with rest or nitroglycerin. Stable angina usually has a stable pattern of onset, duration, severity, and relieving factors. 2. Unstable angina

Unstable angina also is called preinfarction angina. Unstable angina occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration, and severity over time.

 Pain may not be relieved with nitroglycerin. 3. Variant angina

Variant angina also is called Prinzmetals or vasospastic angina. Variant angina results from coronary artery spasm. Variant angina may occur at rest. Attacks may be associated with ST segment elevation noted on the electrocardiogram. 4. Intractable angina is a chronic, incapacitating angina that is unresponsive to interventions. 5. Preinfarction angina

Preinfarction angina is associated with acute coronary insufficiency. Preinfarction angina lasts longer than 15 minutes. Preinfarction angina is a symptom of worsening cardiac ischemia. 6. Postinfarction angina occurs after an MI, when residual ischemia may cause episodes of angina.

Risk Factors
Atherosclerosis Hypertension Diabetes Mellitus Thromboangitis Obliterans Polycythemia Vera Aortic Regurgitation

Assessment
1. Pain a. Pain can develop slowly or quickly. b. Pain usually is described as mild or moderate. c. Substernal, crushing, squeezing, pain may occur. d. Pain may radiate to the shoulders, arms, jaw, neck, and back. e. Pain usually lasts less than 5 minutes, however, pain can last up to 15 to 20 minutes. f. Pain is relieved by nitroglycerin or rest. 2. Dyspnea 3. Pallor 4. Sweating 5. Palpitations and tachycardia 6. Dizziness and faintness 7. Hypertension

8. Digestive disturbances

Diagnostic Evaluation
1. Electrocardiogram: Readings are normal during rest, with ST depression or elevation and/or T wave inversion during an episode of pain. 2. Stress test: Chest pain or changes in the electrocardiogram or vital signs during testing may indicate ischemia. 3. Cardiac enzymes and troponins: Findings are normal in angina. 4. Cardiac catheterization: Catheterization provides a definitive diagnosis by providing information about the patency of the coronary arteries.

Primary Nursing Diagnosis

Altered tissue perfusion (myocardial) related to narrowing of the coronary artery(ies) and associated with atherosclerosis, spasm, or thrombosis

Other Diagnoses that may occur in Nursing Care Plans For Angina Acute pain Risk for decreased cardiac output Anxiety Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs

Medical Management
The goals of medical management are to decrease the oxygen demands of the myocardium and to increase the oxygen supply through pharmacologic therapy and risk factor control. Surgical Management Frequently, therapy includes a combination of medicine and surgery. Surgically, the goals of management include revascularization of the blood supply to the myocardium.

Coronary artery bypass surgery or minimally invasive direct coronary artery bypass (MIDCAB) Percutaneous transluminal coronary angioplasty (PTCA) or percutaneous transluminal myocardial revascularization (PTMR) Application of intracoronary stents and atherectomy to enhance blood flow Lasers to vaporize plaques Percutaneous coronary endarterectomy to extract obstruction.

Pharmacologic Intervention
Nitrates, the mainstay of therapy (nitroglycerin) Beta-adrenergic blockers (metoprolol [Toprol]) Calcium ion antagonists and calcium-channel blockers (amlodipine [Norvase] and diltiazem [Cardizem]) Antiplatelet and anticoagulant medications (aspirin, clopidogrel (Plavix], ticlopidine [Ticlid], or heparin) Oxygen therapy

Nursing Intervention
Immediate management

1. 2. 3. 4.

Assess pain. Provide bed rest. Administer oxygen at 3 L/min by nasal cannula as prescribed. Administer nitroglycerin as prescribed to dilate the coronary arteries, reduce the oxygen requirements of the myocardium and relieve the chest pain. 5. Obtain a 12-Lead electrocardiogram. 6. Provide continuous cardiac monitoring. Following acute episode:

1. Instruct the client regarding the purpose of diagnostic medical and surgical procedures and the preprocedure and postprocedure expectations. 2. Assist the client to identify angina precipitating events. 3. Instruct the client to stop activity and rest if chest pain occurs and to take nitroglycerin as prescribed. 4. Instruct the client to seek medical attention if pain persists. 5. Instruct the client regarding prescribed medications. 6. Provide diet instructions o the client, stressing that dietary changes are not temporary and must be maintained or life. 7. Assist the client to identify risk factors that can be modified. 8. Assist the client to set goals that will promote changes in lifestyle to reduce the impact of risk factors. 9. Assist the client to identify barriers to compliance with therapeutic plan and to identify methods to overcome barriers. 10. Provide community resources to the client regarding exercise, smoking reduction, and stress reduction.

Documentation Guidelines

Description of pain: Onset (sudden, gradual), character (aching, sharp, burning, pressure), precipitating factors, associated symptoms (anxiety, dyspnea, diaphoresis, dizziness, nausea, cyanosis, pallor), duration, and alleviating factors of the anginal episode Response to prescribed medications Reaction to bedrest or limitation in activity

Discharge and Home Healthcare Guidelines

PREVENTION. Teach the patient factors that may precipitate anginal episodes and the appropriate measures to control episodes. Teach the patient the modifiable cardiovascular risk factors and ways to reduce them. Manage risk factors, including hypertension, diabetes mellitus, obesity, and hyperlipidemia. ACTIVITY. Each person has a different level of activity that will aggravate anginal symptoms. Most patients with stable angina can avoid symptoms during daily activities by reducing the speed of any activity. MEDICATIONS. Be sure the patient understands all medications, including the dose, route, action, and adverse effects. If the patients physician prescribes sublingual nitroglycerin (NTG), instruct the patient to lie in semi-Fowler position and take up to three tablets 5 minutes apart to relieve chest discomfort. Instruct the patient that if relief is not obtained after ingestion of the three tablets, he or she should seek medical attention immediately. Remind the patient to check the expiration date on the NTG tablets and to replace the bottle, once it is opened, every 3 to 5 months. COMPLICATIONS. Teach the patient the importance of not denying or ignoring angina episodes and of reporting them to the healthcare provider immediately.

MYOCARDIAL INFARCTION

Description
Refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow. The affected muscle tissue subsequently becomes necrotic. Onset of Myocardial Infarction may be sudden or gradual, and the process takes 3 to 6 hours to run its course. It is the most serious manifestation of acute coronary syndrome, a complication of coronary artery disease (CAD). Approximately 90% of Myocardial Infarction are precipitated by acute coronary thrombosis (partial or total) secondary to severe CAD (greater than 70% narrowing of the artery). Other causative factors include coronary artery spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart in the presence of significant coronary artery disease.

Risk Factors
Modifiable

Infarctions may occur for a variety of reasons, but coronary thrombosis of a coronary artery narrowed with plaque is the most common cause. Other causes include spasms of the coronary arteries; blockage of the coronary arteries by embolism of thrombi, fatty plaques, air, or calcium; and disparity between myocardial oxygen demand and coronary arterial supply. Multiple risk factors have been identified for coronary artery disease and MI.

Modifiable risk factors include cigarette smoking, which causes arterial vasoconstriction and increases plaque formation. A diet high in saturated fats, cholesterol, sugar, salt, and total calories increases the risk for MIs. Elevated serum cholesterol and low-density lipoprotein levels increase the chance for atherosclerosis. Hypertension and obesity increase the workload of the heart, and diabetes mellitus decreases the circulation to the heart muscle. Hostility and stress may also increase sympathetic nervous system activity and pose risk. A sedentary lifestyle diminishes collateral circulation and decreases the strength of the cardiac muscle. Medications can also prevent risks. Oral contraceptives may enhance thrombus formation, cocaine use can cause coronary artery spasm, and anabolic steroid use can accelerate atherosclerosis.

Non-Modifiable

Some factorssuch as age, family history, and gendercannot be modified. Aging increases the atherosclerotic process, family history may increase the risk by both genetic and environmental influences, and males are more prone to MIs than are premenopausal women. Premenopausal women have the benefit of protective estrogens and a lower hematocrit, although heart disease is on the rise in this population, possibly because of an increased rate of smoking in women. Once women become postmenopausal, their risk for MI increases, as it also does for men over age 50.

Assessment
1. Chest pain o Character: variable, but often diffuse, steady substernal chest pain. Other sensations include a crushing and squeezing feeling in the chest. Other sensations include a crushing and squeezing feeling in the chest. o Severity: pain may be severe; not relieved by rest or sublingual vasodilator therapy, requires opioids. o Location: variable, but often pain resides behind upper or middle third of sternum. o Radiation: pain may radiate to the arms (commonly the left), and to the shoulders, neck, back, or jaw. o Duration: pain continues for more than 15 minutes. 2. Associated manifestations include anxiety, diaphoresis, cool clammy skin, facial pallor, hypertension or hypotension, bradycardia or tachycardia, premature ventricular or atrial beats, palpitations, dyspnea, disorientation, confusion, restlessness, fainting, marked weakness, nausea, vomiting, and hiccups. 3. Atypical symptoms of MI include epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, and extreme fatigue (more frequent in women). 4. Risk factors for MI include male gender, age over 45 for men, age over 55 for men, smoking; high blood cholesterol levels, hypertension, family history of premature CAD, diabetes and obesity.

Primary Nursing Diagnosis

Altered tissue perfusion (myocardial) related to narrowing of the coronary artery(ies) associated with atherosclerosis, spasm, or thrombosis

Diagnostic Evaluation
1. Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72 to 96 hours. o ST-segment depression and T-wave inversion indicate a pattern of ischemia; ST elevation indicates an injury pattern. o Q waves indicate tissue necrosis and are permanent. 2. Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated. 3. More specific creatinine phosphokinase isoenzyme CK-MB will be elevated. 4. Triponin T and I are myocardial proteins that increase in the serum about 3 to 4 hours after an MI, peak in 4 to 24 hours, and are detectable for upto 2 weeks; the test is easy to run, can help diagnose an MI up to 2 weeks earlier, and only unstable angina causes a false positive. 5. White blood cell count and sedimentation rate may be elevated. 6. Radionuclide imaging, positron emission tomography, and echocardiography may be done to evaluate heart muscle.

Medical Management
The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications such as lethal dysrrhythmias and cardiogenic shock.

Oxygen administration is initiated at the onset of chest pain. Reperfusion via emergency use of thrombolytic medications or percutaneous coronary interventions (PCI). Coronary artery bypass or minimally invasive direct coronary bypass (MIDCAB).

Medications

Analgesic 1. For relief of pain. This is a priority. Pain may cause shock. 2. Morphine Sulfate. Lidocaine or Nitroglycerine administered intravenously. Thrombolytic Therapy: 1. To disitegrate blood clot by activating the fibrinolytic processes. 2. Streptokinase, urokinase and tissue plasminogen activator (TPA) are currently used.

3. Adminstration is most crucial between 3 to 6 hours after the initial infarction has occurred. 4. Detect for occult bleeding during and after thrombolytic therapy 5. Assess neurologic status changes which may indicate G.I. bleeding or cardiac tamponade. Anticoagulant and antiplatelet medications are administered after thrombolytic therapy to maintain arterial patency. Other medications: Beta-adrenergic blockings agents; diazepam (Valium)

Pharmacologic Intervention
1. Pain control drugs to reduce catecholamine-induced oxygen demand to injured heart muscle. o Opiate analgesics: Morphine o Vasodilators: Nitroglycerin o Anxiolytics: Benzodiazepines 2. Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction. 3. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy. 4. Reperfusion arrhythmias may follow successful therapy. 5. Beta-adrenergic blockers, to improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart, and provide antiarrhythmic effects. 6. Calcium channel blockers, to improve oxygen supply and demand.

Nursing Interventions
1. Monitor continuous ECG to watch for life threatening arrhythmias (common within 24 hours after infarctions) and evolution of the MI (changes in ST segments and T waves). Be alert for any type of premature ventricular beats- these may herald ventricular fibrillation or ventricular tachycardia. 2. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Also monitor blood pressure continuously when giving nitroglycerin I.V. 3. Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring. 4. Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension. 5. Emphasize the importance of reporting any chest pain, discomfort, or epigastric distress without delay. 6. Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment. 7. Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest. 8. Take measures to prevent bleeding if patient is thrombolitic therapy 9. Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinations, diminished pain tolerance, and aggressiveness.

10. Tell the patient that sexual relations may be resumed on advise of health care provider, usually after exercise tolerance is assessed.

Documentation Guidelines
Response to vasodilators and pain medications Physical findings of cardiac functions: Vital signs, heart sounds, breath sounds, urine output, peripheral pulses, level of consciousness Psychosocial response to treatment and diagnosis Presence of complications: Bleeding tendencies, respiratory distress, unrelieved chest pain, constipation

Discharge and Home Healthcare Guidelines

Be sure the patient understands all the medications, including the dosage, route, action, and adverse effects. Instruct the patient to keep the nitroglycerin bottle sealed and away from heat. The medication may lose its potency after the bottle has been opened for 6 months. If the patient does not feel a sensation when the tablet is put under the tongue or does not get a headache, the pills may have lost their potency. Explain the need to treat recurrent chest pain or MI discomfort with sublingual nitroglycerin every 5 minutes for three doses. If the pain persists for 20 minutes, teach the patient to seek medical attention. If the patient has severe pain or becomes short of breath with chest pain, teach the patient to take nitroglycerin and seek medical attention right away. Explore mechanisms to implement diet control, an exercise program, and smoking cessation if appropriate.

The effect of myocardial damage on the pumping ability of the heart and the sequelae of events that would follow decreased pumping ability. MI ==>damaged heart muscle ==>lowered ejection fraction ==>decreased blood pumping out==>kidneys can "sense" the reduction in flow and all of the compensatory mechanisms are initiated. The renin-angiotensin-aldosterone system comes into play==>body conserves fluid in an attempt to increase the total volume. These compensatory mechanisms work fine in the short run, but after awhile this increase in total volume puts an even greater workload on the heart and leads to congestive heart failure. You should focus your research on the electrolytes involved in these processes (Na, K. etc.) Also, realize that an acute loss of blood supply to the cardiac muscle causes rapid depletion of potassium from the ischemic musculature (from Guyton textbook of

Phys.), this increases potassium in the extracellular fluids surrounding the cardiac muscle fibers and in turn increases the irritability of the heart.

3 areas which develop in MI ZONE OF INFARCTION-records pathologic Q wave in the ECG ZONE OF INJURY- gives rise to elevated ST segment ZONE OF ISCHEMIA- produces inversion of T wave

Classification of Mi Transmural infarct-extends from endocardium to epicardium Subendocardial infarct- affects the endocardial muscles Intramural infarction- seen in patchy areas of the myocardium ;equally associated with angina pectoris

Mechanisms of Occlusion

Most MIs are caused by a disruption in the vascular endothelium associated with anunstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, whichresults in coronary artery blood flow occlusion. If such an occlusion persists long enough (20 to40 min), irreversible myocardial cell damage and cell death will occur. The development of atherosclerotic plaque occurs over a period of years to decades. Theinitial vascular lesion leading to the development of atherosclerotic plaque is not known withcertainty. The two primary characteristics of the clinically symptomatic atherosclerotic plaqueare a fibromuscular cap and an underlying lipid-rich core. Plaque erosion may occur due to theactions of metalloproteases and the release of other collagenases and proteases in the plaque,which result in thinning of the overlying fibromuscular cap. The action of proteases, in additiont o h e m o d y n a m i c f o r c e s a p p l i e d t o t h e a r t e r i a l s e g m e n t , c a n l e a d t o a d i s r u p t i o n o f t h e endothelium and fissuring or rupture of the fibromuscular cap. The degree of disruption of theoverlying endothelium can range from minor erosion to extensive fissuring that results in anulceration of the plaque. The loss of structural stability of a plaque often occurs at the juncture of the fibromuscular cap and the vessel walla site otherwise known as the plaque's "shoulder r e g i o n . " A n y a m o u n t o f d i s r u p t i o n o f t h e e n d o t h e l i a l s u r f a c e c a n c a u s e t h e f o r m a t i o n o f thrombus via platelet-mediated activation of the coagulation cascade. If a thrombus is largeenough to completely occlude coronary blood flow for a sufficient time period, MI can result. Mechanisms of Myocardial Damage The severity of an MI is dependent on three factors: the level of the occlusion in thecoronary artery, the length of time of the occlusion, and the presence or absence of collateralcirculation. Generally speaking, the more proximal the coronary occlusion, the more extensive isthe amount of myocardium at risk of necrosis. The larger the MI, the greater is the chance of death due to a mechanical complication or pump failure. The longer the time period of vesselocclusion, the greater the chances of irreversible myocardial damage distal to the occlusion. The death of myocardial cells first occurs in the area of myocardium that most distal tothe arterial blood supplythat is, the endocardium. As the duration of the occlusion increases,the area of myocardial cell death enlarges, extending from the endocardium to the myocardium and ultimately to the epicardium. The area of myocardial cell death then spreads laterally to areasof watershed or collateral perfusion. Generally, after a 6- to 8-hour period of coronary occlusion,m o s t o f t h e d i s t a l m y o c a r d i u m h a s d i e d . T h e e x t e n t o f m y o c a r d i a l c e l l d e a t h d e f i n e s t h e magnitude of the MI. If blood flow can be restored to atrisk myocardium, more heart muscle can be saved from irreversible damage or death

CORONARY ARTERY DISEASE Description

Is characterized by the accumulation of plaque within coronary arteries, which progressively enlarge, thicken and calcify. This causes critical narrowing of the coronary artery lumen (75% occlusion), resulting in a decrease in coronary blood flow and an inadequate supply of oxygen to the heart muscle. Ischemia may be silent (asymptomatic but evidenced by ST depression of 1 mm or more on electrocardiogram (ECG) or may be manifested by angina pectoris (chest pain). Risk factor for Coronary Artery Disease include dyslipidemia, smoking, hypertension, male gender (women are protected until menopause), aging, non-white race, family history, obesity, sedimentary lifestyle, diabetes mellitus, metabolic syndrome, elevated homocysteine, and stress. Acute coronary syndrome is a complication of CAD due to lack of oxygen to the myocardium. Mnaifestations include unstable angina, non ST-segment elevation infarction, and ST-segment elevation infarction. Other causes of angina include coronary artery spasm, aortic stenosis, cardiomyopathy, severe anemia, and thyrotoxicosis.

Risk Factors

Modifiable

Cigarette smoking Elevated blood pressure High blood cholesterol (hyperlipidemia) Hyperglycemia (diabetes mellitus) Obesity Physical inactivity Use of oral contraceptives Infection (e.g., gingivitis): possibly associated Behavior patterns ( stress, aggressiveness, hostility) Geography: higher incidence in industrialize regions

Non-modifiable

Positive family history ( first degree relative with cardiovascular disease at age 55 or less for males at age 65 or less for female Age ( more than 45 yrs. for men, more than 55 yrs for women) Gender ( occurs 3 times more often in men than in women) Race: higher incidence in Africans Americans than in Caucasian.

Assessment
Chest pain is provoked by exertion or stress and is relieved by nitroglycerin and rest.

1. Character. Substernal chest pain, pressure, heaviness, or discomfort. Other 2. 3. 4. 5. 6. 7.

8. sensations include a squeezing, aching, burning, choking, strangling, or cramping pain. Severity. Pain maybe mild or severe and typically present with a gradual buildup of discomfort and subsequent gradual fading away. Location. Behind middle or upper third of sternum; the patient will generally will make a fist over the site of pain (positive Levine sign; indicates diffuse deep visceral pain), rather than point to it with fingers. Radiation. Usually radiates to neck, jaw, shoulders, arms, hands, and posterior intrascapular area. Pain occurs more commonly on the left side than the right; may produce numbness or weakness in arms, wrist, or hands. Duration. Usually last 2 to 10 minutes after stopping activity; nitroglycerin relieves pain within 1 minute. Precipitating factors. Physical activity, exposure to hot or cold weather, eating a heavy meal, and sexual intercourse increase the workload of the heart and, therefore, increase oxygen demand. Associated manifestation. Diaphoresis, nausea, indigestion, dyspnea, tachycardia, and increase in blood pressure. Signs of unstable angina: A change in frequency, duration, and intensity of stable angina symptoms.

 Angina pain last longer than 10 minutes, is unrelieved by rest or sublingual nitroglycerin, and mimics signs and symptoms of impending myocardial infarction.

Diagnostic Evaluation
1. Resting ECG may show left ventricular hypertrophy, ST-T changes, arrhythmias, and possible Q waves. 2. Exercise stress testing with or without perfusion studies shows ischemia. 3. Cardiac catheterization shows blocked vessels. 4. Position emission tomography may show small perfusion defects. 5. Radionuclide ventriculography shows wall motion abnormalities and ejection fraction. 6. Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein, lipoprotein A, homocysteine, and triglycerides may be abnormal. 7. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies.

Primary Nursing Diagnosis

Altered tissue perfusion (myocardial) related to narrowing of the coronary artery(ies) associated with atherosclerosis, spasm, and/or thrombosis

Other Diagnoses that may occur in Nursing Care Plans For CAD Acute pain Risk for decreased cardiac output Anxiety Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs

Medical Management
The goals of medical management are to decrease the oxygen demands of the myocardium and to increase the oxygen supply through pharmacological therapy and risk factor control Surgical Interventions

1. Percutaneous transluminal coronary angioplasty or intracoronary atherectomy, or placement of intracoronarystent. 2. Coronary artery bypass grafting. 3. Transmyocardial revascularization.

Pharmacologic Intervention
1. Antianginal medications (nitrates, beta-adrenergic blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors) to promote a favorable balance of oxygen supply and demand. 2. Antilipid medications to decrease blood cholesterol and tricglyceride levels in patients with elevated levels. 3. Antiplatelet agents to inhibit thrombus formation. 4. Folic acid and B complex vitamins to reduce homocysteine levels.

Nursing Intervention
1. Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an anginal attack. 2. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for arrhythmias and ST elevation. 3. Place patient in comfortable position and administer oxygen, if prescribed, to enhance myocardial oxygen supply. 4. Identify specific activities patient may engage in that are below the level at which anginal pain occurs. 5. Reinforce the importance of notifying nursing staff whenever angina pain is experienced. 6. Encourage supine position for dizziness caused by antianginals. 7. Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and calcium channel blocker therapy. These drug must be tapered to prevent a rebound phenomenon; tachycardia, increase in chest pain, and hypertension. 8. Explain to the patient the importance of anxiety reduction to assist to control angina. 9. Teach the patient relaxation techniques. 10. Review specific factors that affect CAD development and progression; highlight those risk factors that can be modified and controlled to reduce the risk.

Documentation Guidelines

Episodes of angina describing character, location, and severity of pain; precipitating or mitigating factors; interventions; and evaluation Patient teaching about disease process and planned treatments, including medication regimen Perioperative hemodynamic response: Pulmonary and systemic arterial pressures, presence of pulses, capillary refill, urine output Pulmonary assessment: Breath sounds, ventilator settings, response to mechanical ventilation, secretions Complications: Bleeding, blood gas alterations, fluid volume deficit, hypotension, dysrhythmias, hypothermia Coping: Patient and family Mediastinal drainage and autotransfusion

Discharge and Home Healthcare Guidelines

PREVENTION. Review the risk factor and lifestyle modifications that are acceptable to the patient and her or his family members. MEDICATIONS. Be certain that the patient and appropriate family members understand all medications, including the correct dosage, route, action, and adverse effects. PERIOPERATIVE o Care of Incision. Often the incision heals with no home healthcare, but the patient needs to know the signs of infection. o Activity Restrictions. The activity recommendations will depend on the type and extent of the patients underlying condition.