Angina and MI PDF

 ANGINA PECTORIS/MYOCARDIAL ISCHEMIA Insufficient blood flow resulting to inadequate oxygen supply to the myocardium causing transient chest pain due to obstruction or spasm of coronary arteries  CAUSES ATHE...

 ANGINA PECTORIS/MYOCARDIAL ISCHEMIA Insufficient blood flow resulting to inadequate oxygen supply to the myocardium causing transient chest pain due to obstruction or spasm of coronary arteries  CAUSES ATHEROSCLEROSIS PATHOPHYSIOLOGY OF ANGINA PECTORIS HYPERTENSION DIABETES MELITUES THROMBOANGITIS OBLITERANS POLYCYTHEMIA VERA AORTIC REGURGITATION REDUCED CORONARY TISSUE DIMINISHED MYOCARDIAL OXYGENATION ANAEROBIC METABOLISM INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS ) CHEST PAIN  Types of Angina Pectoris Stable Angina the most common form of angina characterized by burning, heavy, or squeezing feeling in the chest.  Types of Angina Pectoris Unstable angina chest pains occur with increased frequency requires hospital admission and more aggressive therapy  Types of Angina Pectoris STABLE ANGINA UNSTABLE ANGINA Chest pain last for less than Chest pain is last more than 15 15 minutes minutes but not more than 30 minutes Recurrence is less frequent Recurrence is more frequent Relieved by Rest or not relieve by rest or nitroglycerin nitroglycerin.  Types of Angina Pectoris Prinzmetal’s or Vasospastic Angina Is uncommon pattern of episodic angina that occurs at rest due to coronary artery spasm. Responds promptly to coronary vasodilators and calcium-channel blockers.  Intractable Angina Also called Refractory Angina Chronic incapacitating angina unresponsive to intervention. Respond poorly invasive procedures such as angioplasty or by pass surgeries. Nocturnal Angina Occurs only at night and possibly associated with REM sleep Angina Decubitus Paroxysmal chest pain that occurs in sitting or lying down Post infarction angina Occurs after MI, when residual ischemia may cause episodes of angina.  Precipitating factors of Angina 4 E’s Exertion Emotion Eating heavy meal Environment  Clinical Manifestations Chest pain Transient (temporary), paroxysmal substernal or pre cordial pain, squeezing, burning, pressing, choking aching or bursting left sternal chest pain Heaviness or chest tightness The patient often says, “It feels like gas or heartburn or indigestion” Radiates down one or both arms, left shoulder jaw, neck and back Precipitated by physical exertion Relieve by rest and Nitroglycerine  Assessment of Chest Pain Precipitating factors of Angina Provocative Quality Region Severity Timing and Treatment SUBSEQUENT ASSESSMENT Obtain 12 lead ECG Assess patient knowledge on the disease Medical history Drug therapy Clinical Manifestations Pallor Diaphoresis Dyspnea Faintness Palpitation Dizziness  NURSING INTERVENTIONS Assess the level of chest pain and its duration Place in comfortable position VS q 5-10 minutes until anginal pain subsides Administer oxygen and Nitroglycerine as ordered Monitor relief of pain NURSING INTERVENTIONS To maintain C.O. Instruct to avoid over fatigue Stop activity immediately Monitor BP and HR in response to drug therapy Institute continuous ECG  To Decrease Anxiety Minimize emotional outburst, worry and tension Verbalize fears and concerns Maintain an optimistic outlook Explain the reasons for hospitalization, diagnostic test, and therapies administered Teach relaxation techniques such as yoga, DBE Administer sedative and tranquilizer. DIET Low sodium, low fat and cholesterol, High Fibers Avoid saturated fat (animal fats) White meat ( chicken without skin, turkey, fish are low in cholesterol) Read labels  MYOCARDIAL INFARCTION (MI) Results from prolonged lack of blood flow to a portion of the myocardial tissue resulting to lack of OXYGEN, DEATH or NECROSIS to the myocardial tissue. PATHOPHYSIOLOGY OFATHEROSCLEROSIS, ANGINA CAUSES PECTORIS Thrombosis, REDUCED CORONARY TISSUE DIMINISHED MYOCARDIAL OXYGENATION Left atrium and ventricle INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS ) Ischemia, injury, Necrosis What happens to the heart muscle after an MI? Early signs of an MI no physical changes to heart muscle yet (until about 6-8 hours). If the myocytes die cardiac enzymes are released: CK-MB (4 to 6 hours after MI), troponin (2-4 hour most regarded) myoglobin (1 hour after injury)  Within 24-36 hours inflammation sets in and neutrophils come on the scene and congregate at the damaged tissue site. complication is possible pericarditis. within 24 hours the heart fails to pump efficiently resulting to cardiogenic shock and arrhythmias Within 10 days granulation occurs when the macrophages come on the scene. WBCs came to clean up the dead cells and other components. The new tissue formed from granulation is not well formed and is weak. This increases the chance of cardiac rupture. Within 2 months scarring occurs, and the heart is affected in size and functionality due to increased collagen.  ETIOLOGY/CAUSES Thrombus formation- the most common causes of MI Severe CAD Intramural hemorrhage Coronary artery spasm Coronary artery embolism  Degree of Damage to the Heart Muscle Myocardial ischemia/Zone of ischemia ❖ Temporary deprivation of oxygen and transient absence of blood supply and other nutrients to the heart Degree of Damage to the Heart Muscle Myocardial injury/zone of injury ❖ Inflamed and Damage to the heart muscle (myocardium) ❖ Most commonly results from myocardial ischemia Degree of Damage to the Heart Muscle Myocardial Necrosis/Zone of infarction ❖ Death of myocardial tissue (MI) ❖ Complete oxygen deprivation ❖ Irreversible damage  Classification of MI according to the Heart muscle involve Transmural (Q wave) infarction ❖ necrosis occurs throughout the entire thickness of the heart muscle ❖ extends from endocardium to epicardium  Classification of MI according to the Heart muscle involve Sub endocardial infarction ❖ necrosis is in the innermost layer of the heart lining chambers. ❖ Affects the endocardial muscles Intramural infarction ❖ patchy areas of the myocardium associated with long standing angina pectoris.  ANGINA AND MI ANGINA PECTORIS MI Chest pain- usually last less 15 Chest pain-last more than 2 minutes hours Relieve by nitroglycerine Not relieve by nitroglycerine Nitroglycerine Morphine Precipitated by stress and Not exercise Relieve by rest Not Maybe accompanied by Accompanied by dysrhythmias dysrhythmias  Clinical Manifestations Chest pain (intense, heavy) Radiating chest pain that goes to left arm, jaw, back Unrelieved by nitroglycerin or rest (chest pain) Sweating (cold) Hard to breathe (shortness of breath) Increased heart rate, blood pressure or irregular heart rate Nausea with vomiting Going to be anxious and scared  CLINICAL MANIFESTATIONS Shock- hypotension, tachycardia-bradycardia, tachypnea, lethargy, cold skin and diaphoresis, peripheral cyanosis and weak pulse. Anxiety and Apprehension Oliguria FEVER Suffocation, dyspnea, orthopnea, gurgling or bubbling respiration  Diagnostic Evaluations ECG changes Elevation of ST segment- results from injury area or Acute MI Inverted T wave- From the zone of ischemia Pathologic Q wave- Develops due to area of infarction/tissue necrosis and are permanent Elevated Troponins gold standard now used by most hospitals in assessing for an MI Most specific test to detect MI. Elevated Troponin T, I, C- sensitive as CK MB for the detection of MI usually drawn every 6 hours for 3 sets. CK-MB it elevates 4-6 hr after injury the most sensitive enzyme for determining for heart muscle damage Elevated LDH 1 and LDH 2 sensitive isoenzyme that indicates myocardial damage Elevated WBC and ERS due to inflammatory process  OTHER TEST Echocardiogram Heart Catheterization Stress test with Myocardial Perfusion Imaging  Nursing Interventions Monitoring & Assessing Cardiovascular system-12-lead EKG, and continuous bedside cardiac monitoring. Semi fowlers OXYGEN via nasal cannula- at 2- 4 L/Minute Working IV access Monitor lung sounds “crackles” Bedrest for 24-48hrs  Nursing Interventions Collect cardiac enzymes as ordered by the physician Administering medications per MD order: Oxygen, Morphine sulphate, MEPERIDINE (DEMEROL), THROMBOLYTIC THERAPY Streptokinase (streptase), Urokinase, and Tissue plasminogen activator (Activase). MORPHINE SULFATE Narcotic Agonist, analgesic, DOC of MI Used relieve pain To improve hemodynamics by reducing pre load and afterload and promotes venous pooling of blood in the periphery  NURSING CONSIDERATIONS Best taken with Food Report nausea and vomiting and respiratory depression Keep Naloxone HCL (antidote) at the bedside Instruct the patient to lie down during IV administration. Contraindicated to patient with PANCREATITIS MEPERIDINE (DEMEROL) Narcotic Analgesic Has Vagolytic effect resulting to increase myocardial oxygen demand Negative Pain Avoid alcohol Keep the antidote Naloxone hydrochloride Supine position- prevent hypotension  THROMBOLYTIC THERAPY Streptokinase (streptase), Urokinase, and Tissue plasminogen activator (Activase) It dissolve obstructing thrombus Detect for occult bleeding during and after thrombolytic therapy Assess neurologic status changes  ANTI-THROMBOTIC AGENTS prevent formation of clot Lovenox and Heparin monitor for bleeding (assess gums of mouth, stool (dark tarry), drop in blood pressure and increase in heart rate, blood in urine watch platelet count which may start to decrease after several days  ANTI PLATELET It decrease platelets aggregation and thrombus formation It prevents platelet from clumping and blood clots from forming Aspirin (ASA), Plavix, Dypiridamole, Clopidogril Watch for signs and symptoms of GI bleeding, and Thrombotic Thrombocytopenic Purpura (TTP)  NSG CONSIDERATIONS Watch for signs and symptoms of GI bleeding, especially if patient has a history. Assess for ss and sx of bleeding Avoid straining of stool. ASA with food. Observe for TINNITUS. ASA toxicity ASA may cause Bronchoconstriction.  Anti-Coagulants It prevent blood clotting Inactivates thrombin and other clotting factors inhibiting conversion of fibrinogen to fibrin Examples: Heparin, Coumadin Heparin Sodium ▪ Assess for signs of bleeding ▪ Keep protamine sulfate at the bedside. ▪ If administered SC, do not aspirate and massage the site of heparin injection. ▪ Monitor PTT or APTT levels ▪ Used for maximum of 2 weeks  Warfarin Sodium (Coumadin) Assess for signs of bleeding Keep Vit K. Antidote if bleeding occurs in Coumadine therapy Monitor Prothrombin Time Minimize green leafy vegetables in the diet. Don’t give ASA and Coumadin together to prevent bleeding.  NITROGLYCERINE Promotes venous and arterial relaxation of coronary vessel and prevention of coronary spasm causes vasodilation and increases blood flow to the heart, hence better blood flow to the area experiencing ischemia ointment, sublingual, IV, patch, or oral “Imdur” Relief of chest pain  NURSING CONSIDERATONS Best taken before any strenuous activity Place a tablet under the tongue at the first sign of chest pain. Burning sensation is a sign of potency of the drug. Facial flushing is a side effect. Do not chew the tablet. Keep the tablets in dark container. Monitor the BP and HR.  Ace Inhibitors ends in “pril” Lisinopril, Ramipril, Enalapril, Captopril It work by allowing more blood to get to the heart muscle It does this by blocking the conversion of Angiotensin I or Angiotensin II  Beta Adrenergic Blocking Agent ends with “lol” decrease myocardial oxygen demand by decreasing the heart rate, bp, myocardial contractility and calcium output. Propanolol, Atenolol, Metoprolol, Esmolol, Nadolol, Pindolol, Timolol  NURSING CONSIDERATION (BETA-BLOCKERS) Assess the PR before giving the drug. Best taken with food Do not give to clients with asthma and DM patients Observe for SE: NV, mental depression, mild diarrhea, fatigue, impotence. GLUCAGON- antidote for beta blocker poisoning. ARBS Angiotensin II Receptor Blockers end in “sartan” like Losartan, Valsartan It blocks angiotensin II receptors which causes vasodilation. Monitor sodium, K, and blood pressure Statins (“tins) Simvastatin, Atorvastatin, helps lower LDL, total cholesterol, triglycerides, and increase HDL. Educate not to replace diet and exercise Notify doctor if they develop muscle pain or tenderness Monitor CPK (creatine kinase) levels if elevated Monitor liver function  Calcium Channel Blockers Norvasc, Cardizem, Verapamil (Isoptin, Calan), Amlodipine, Nicardipine, Nifedipine, Diltiazem stops the transport of calcium to the myocardium and into smooth muscle which causes vasodilation on the coronary arteries to Improve oxygen demand and supply Monitoring heart rate, orthostatic hypotension, Educate about good oral hygiene  NURSING CONSIDERATIONS Assess HR and BP Monitor hepatic and renal function Administer 1 hr before or 2 hrs after meal. Prepare GLUCAGON- antidote for calcium channel blocker overdose  Surgical Management Percutaneous Transluminal Coronary Angioplasty A balloon tip catheter is placed in a coronary vessel narrowed by plaque The balloon is inflated and deflated to stretch the vessel and flatten the lesion Blood flows freely through the unclogged vessel to the heart.  Surgical Management Intra Coronary Stent A diamond mesh tubular device is placed in the coronary artery Prevents re-stenosis (after PTCA) by providing skeletal support  Surgical Management Intra Coronary Atherectomy A blade tip catheter is guided in a coronary vessel to the site of the plaque The plaque is cut, shave, or pulverized then removed  Surgical Management Coronary Artery Bypass Graft A graft is surgically attached to the aorta and the other end of the graft is attached to a distal portion of a coronary vessel. By passes obstructive lesion in the vessel and returns to adequate blood flow to the heart muscle supplied by the artery. Self Management Education Guide To Decrease the Anginal Attack and MI Manage Hypertension Avoid extreme activities such Stop active and passive as sudden exertion, walking smoking against the wind, extreme temperature, high altitude, Avoid alcohol emotionally stressful situations Avoid stress Lose weight if overweight Plan a regular exercise under Healthy diet. medical supervision Adequate time to rest and relaxation