CRITICALLY ILL CLIENTS with ACUTE CORONARY SYNDROMES

ANGINA PECTORIS

 Angina is chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply.

Angina is caused by an imbalance between oxygen supply and demand.

 Causes include obstruction of coronary blood flow because of atherosclerosis, coronary artery spasm, and conditions increasing myocardial oxygen consumption

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
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.

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.

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.

 Intractable angina is a chronic, incapacitating angina that is unresponsive to interventions.

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.

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

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
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. Obtain a 12-Lead electrocardiogram. Provide continuous cardiac monitoring.

Following acute episode:

Instruct the client regarding the purpose of diagnostic medical and surgical procedures and the preprocedure and postprocedure expectations. Assist the client to identify angina precipitating events. Instruct the client to stop activity and rest if chest pain occurs and to take nitroglycerin as prescribed.

 Instruct the client to seek medical attention if pain persists. Instruct the client regarding prescribed medications. Provide diet instructions o the client, stressing that dietary changes are not temporary and must be maintained or life.

 Assist the client to identify risk factors that can be modified. Assist the client to set goals that will promote changes in lifestyle to reduce the impact of risk factors. Assist the client to identify barriers to compliance with therapeutic plan and to identify methods to overcome barriers. Provide community resources to the client regarding exercise, smoking reduction, and stress reduction.

CORONARY ARTERY DISEASE

 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.

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
Character. Substernal chest pain, pressure, heaviness, or discomfort. Other 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.

Non modifiable factors Age Gender Family history

Modifiable factors
Smoking Lack of exercise Stress Diet high in fat Hypertension Elevated Serum cholesterol levels Alcohol consumption Diabetes Mellitus

Non-specific injury to arterial wall (Endothelial Injury)

Desquamation of endothelial lining

Lipids (LDL) and Platelets Assimilate in the Area

Oxydized LDL attracts monocytes and macrophages to the site

Plaques begin to form from cells which imbibed into the endothelium

Plaques are engulfted by cells (foam cells) and smooth muscle cells develop

Disruption of Plaque Continuous aggregation of platelets

Thrombus Formation Rapid increase in size of thrombus in Coronary Artery Wall

Coronary Artery Disease

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

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

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

Nursing Intervention
Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an anginal attack. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for arrhythmias and ST elevation. Place patient in comfortable position and administer oxygen, if prescribed, to enhance myocardial oxygen supply.

 Identify specific activities patient may engage in that are below the level at which anginal pain occurs. Reinforce the importance of notifying nursing staff whenever angina pain is experienced. Encourage supine position for dizziness caused by antianginals.

 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. Explain to the patient the importance of anxiety reduction to assist to control angina. Teach the patient relaxation techniques. Review specific factors that affect CAD development and progression; highlight those risk factors that can be modified and controlled to reduce the risk.

MYOCARDIAL INFARCTION

 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 coronary thrombosis of a coronary artery narrowed with plaque I 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

 cigarette smoking A diet high in saturated fats, cholesterol, sugar, salt, and total calories Hypertension and obesity increase the workload of the heart diabetes mellitus decreases the circulation to the heart muscle.

 Hostility and stress may also increase sympathetic nervous system activity A sedentary lifestyle diminishes collateral circulation and decreases the strength of the cardiac muscle. Oral contraceptives may enhance thrombus formation, cocaine use can cause coronary artery spasm, and anabolic steroid use can accelerate atherosclerosis.

Non-Modifiable
age, family history, and gender Premenopausal women postmenopausal risk for MI increases, as it also does for men over age 50.

Assessment
Chest pain 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. Severity: pain may be severe; not relieved by rest or sublingual vasodilator therapy, requires opioids. Location: variable, but often pain resides behind upper or middle third of sternum. Radiation: pain may radiate to the arms (commonly the left), and to the shoulders, neck, back, or jaw. Duration: pain continues for more than 15 minutes.

Associated manifestations include:

anxiety

Diaphoresis cool clammy skin facial pallor hypertension or hypotension bradycardia or tachycardia vomiting, and hiccups.

premature ventricular or atrial beats Palpitations Dyspnea disorientation, confusion Restlessness Fainting marked weakness nausea,

 Atypical symptoms of MI include:

epigastric or abdominal distress dull aching or tingling sensations shortness of breath extreme fatigue (more frequent in women).

Diagnostic Evaluation
Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72 to 96 hours.
ST-segment depression and T-wave inversion indicate a pattern of ischemia; ST elevation indicates an injury pattern. Q waves indicate tissue necrosis and are permanent.

 Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated.

More specific creatinine phosphokinase isoenzyme CK-MB will be elevated.

 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.

 White blood cell count and sedimentation rate may be elevated. 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
For relief of pain. This is a priority. Pain may cause shock. Morphine Sulfate. Lidocaine or Nitroglycerine administered intravenously.

Thrombolytic Therapy:
To disitegrate blood clot by activating the fibrinolytic processes. Streptokinase, urokinase and tissue plasminogen activator (TPA) are currently used.

 Adminstration is most crucial between 3 to 6 hours after the initial infarction has occurred. Detect for occult bleeding during and after thrombolytic therapy 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
Pain control drugs to reduce catecholamineinduced oxygen demand to injured heart muscle.
Opiate analgesics: Morphine Vasodilators: Nitroglycerin Anxiolytics: Benzodiazepines

 Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy.

 Reperfusion arrhythmias may follow successful therapy. 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.

 Calcium channel blockers, to improve oxygen supply and demand.

Nursing Interventions
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.

 Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Also monitor blood pressure continuously when giving nitroglycerin I.V. Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring.

 Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension. Emphasize the importance of reporting any chest pain, discomfort, or epigastric distress without delay.

 Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment. Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest

 Take measures to prevent bleeding if patient is thrombolitic therapy Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinations, diminished pain tolerance, and aggressiveness. Tell the patient that sexual relations may be resumed on advise of health care provider, usually after exercise tolerance is assessed.

Questions??????