Cardiovascular Disorders Lecture Notes PDF

CARDIOVASCULAR DISORDERS  LEARNING OBJECTIVES: At the end of the lecture, the students will be able to: 1.Identify the major organs and structures of cardiovascular system 2.Discuss the risk factors associated in the development of cardiovascular disorder 3.Discuss the physical assess...

CARDIOVASCULAR DISORDERS  LEARNING OBJECTIVES: At the end of the lecture, the students will be able to: 1.Identify the major organs and structures of cardiovascular system 2.Discuss the risk factors associated in the development of cardiovascular disorder 3.Discuss the physical assessment that provide information about the functioning of the cardiovascular disorder  LEARNING OBJECTIVES: At the end of the lecture, the students will be able to: 4.Describe common diagnostic tests and their nursing responsibilities 5.Discuss the pathophysiology of clients with cardiovascular disorder 6.Enumerate the different clinical manifestations associated with each illness of clients with cardiovascular disorder  LEARNING OBJECTIVES: At the end of the lecture, the students will be able to: 7.Identify actual and at-risk nursing diagnosis 8.Discuss medical and surgical interventions 9.Discuss the appropriate nursing interventions with client/s and family for identified nursing interventions 10.Implement plan of care with clients and family  CARDIOVASCULAR SYSTEM is a closed system consisting of the heart and blood vessels  FUNCTION - to supply body cells and tissues with oxygen-rich blood and eliminate carbon dioxide and cellular wastes HEART - a cone-shaped muscle with four chambers; a double pump about the size of a clenched fist -pumps blood throughout circulatory system RIGHT SIDE RIGHT ATRIUM - upper chamber of right heart - receives unoxygenated blood from superior and inferior vena cava RIGHT SIDE TRICUSPID VALVE -Right AV valve with three cusps (tricuspid) -Valve between right atrium and right ventricle RIGHT SIDE RIGHT VENTRICLE -lower chamber of right heart -receives blood from right atrium and pumps it into pulmonary circuit RIGHT SIDE PULMONARY SEMILUNAR VALVE -composed of three cusps -valve between right ventricle and main pulmonary artery RIGHT SIDE MAIN PULMONARY ARTERY -artery leading from right ventricle to lungs -divides into right and left branches supplying respective lungs -carries unoxygenated blood from right ventricle to lungs RIGHT SIDE PULMONARY VEINS -veins leading from lungs to left atrium -carry oxygenated blood to left atrium LEFT SIDE LEFT ATRIUM - upper chamber of left heart. - receives oxygenated blood from lungs through pulmonary veins LEFT SIDE MITRAL VALVE -AV valve with two cusps (bicuspid) -valve between left atrium and left ventricle LEFT SIDE LEFT VENTRICLE -lower chamber of left half of heart - receives blood from left atrium and pumps oxygenated blood through systemic circulation LEFT SIDE AORTIC VALVE - composed of three cusps - valve between left ventricle and aorta. LEFT SIDE INTERVENTRICULAR SEPTUM - wall between left and right ventricles. - vertically separates left and right sides of heart LAYERS OF THE HEART ENDOCARDIUM - inner layer of heart; a smooth, thin layer of endothelium and connective tissue. -smooth inner lining of the heart LAYERS OF THE HEART MYOCARDIUM - middle and thickest layer of heart; heart muscle. -responsible for cardiac contraction EPICARDIUM - the layer of serous pericardium on heart’s surface. - contains main coronary blood vessels LAYERS OF THE HEART PERICARDIUM - Sac that surrounds the heart and roots of the great vessels. -Composed of two layers: Fibrous pericardium (outer layer of fibrous connective tissue) and serous pericardium SYSTEMIC AND PULMONARY CIRCULATION LAYERS OF ARTERIES AND VEINS ARTERIES - blood vessels with three coats: tunica intima, tunica media, and tunica adventitia. - carry oxygenated blood away from left heart and unoxygenated blood to lungs via pulmonary arteries LAYERS OF ARTERIES AND VEINS ARTERIOLES - Smallest arteries; contain large amount of smooth muscle cells that can dilate and constrict. - Carry blood to capillaries and control blood flow to capillaries through dilation/constriction LAYERS OF ARTERIES AND VEINS CAPILLARIES - Single layer of microscopic endothelial cells. - Connect arterial and venous system for exchange of gases, fluids, nutrients, and wastes. LAYERS OF ARTERIES AND VEINS VEINS - Contain same three layers as arteries, but are thinner with less elastic and collagenous tissue and smooth muscle. - BP in venous system is low; veins have valves to prevent backflow.  - VEINS carry unoxygenated blood back to right heart, except for pulmonary veins, which carry oxygenated blood from lungs to left heart. REGULATION OF HEART RATE - HEART RATE fluctuates according to stimulation from autonomic nervous system, baroreceptors, and chemoreceptors  - AUTONOMIC NERVOUS SYSTEM affects heart rate through sympathetic and parasympathetic nervous system innervation  - SYMPATHETIC NERVE FIBERS, adrenergic neurotransmitters (norepinephrine, epinephrine) excite SA and AV nodes in the conduction system, thus INCREASING HEART RATE  - The same neurotransmitters also stimulate BETA ADRENERGIC RECEPTORS in the atria ventricles, increasing force of myocardial contraction - Heart rate slows when parasympathetic nerve fibers from the cardiac branches of the vagus nerve release the CHOLINERGIC neurotransmitter ACETYLCHOLINE CARDIAC OUTPUT – is the amount of blood pumped out of the left ventricle each minute PROPERTIES OF CARDIAC CYCLE AUTOMATICITY: Generates electrical impulse independently, without involving the nervous system EXCITABILITY: Responds to electrical stimulation PROPERTIES OF CARDIAC CYCLE CONDUCTIVITY: Passes or propagates electrical impulses from cell to cell CONTRACTILITY: Shortens in response to electrical stimulation  ELECTRICAL CONDUCTION SYSTEM OF THE HEART Conduction System Structures and Functions ELECTRICAL CONDUCTION SYSTEM OF THE HEART SINOATRIAL (SA) NODE: Dominant pacemaker of the heart, located in upper portion of right atrium. Intrinsic rate 60–100 bpm. SA NODE ELECTRICAL CONDUCTION SYSTEM OF THE HEART INTERNODAL PATHWAYS: Direct electrical impulses between SA and AV nodes. INTERNODAL PATHWAYS ELECTRICAL CONDUCTION SYSTEM OF THE HEART ATRIO VENTRICULAR (AV) NODE: Part of AV junctional tissue. Slows conduction, creating a slight delay before impulses reach ventricles. Intrinsic rate 40–60 bpm AV NODE ELECTRICAL CONDUCTION SYSTEM OF THE HEART BUNDLE OF HIS: Transmits impulses to bundle branches. Located below AV node BUNDLE OF HIS ELECTRICAL CONDUCTION SYSTEM OF THE HEART LEFT BUNDLE BRANCH: Conducts impulses that lead to left ventricle LEFT BUNDLE BRANCH ELECTRICAL CONDUCTION SYSTEM OF THE HEART RIGHT BUNDLE BRANCH: Conducts impulses that lead to right ventricle RIGHT BUNDLE BRANCH ELECTRICAL CONDUCTION SYSTEM OF THE HEART PURKENJE SYSTEM: Network of fibers that spreads impulses rapidly throughout ventricular walls. Located at terminals of bundle branches. Intrinsic rate 20–40 bpm PURKENJE FIBERS  ELECTROPHYSIOLOGY DEPOLARIZATION: The electrical charge of a cell is altered by a shift of electrolytes on either side of the cell membrane. This change stimulates muscle fiber to contract  ELECTROPHYSIOLOGY REPOLARIZATION: Chemical pumps re- establish an internal negative charge as the cells return to their resting state  Mechanical and electrical functions of the heart are influenced by proper electrolyte balance. Important components of this balance are sodium, calcium, potassium, and magnesium  CARDIO VASCULAR ASSESSMENT  PAST MEDICAL HISTORY REVIEW OF ALLERGIES MEDICATION HISTORY FAMILY HISTORY PERSONAL AND SOCIAL HISTORY  COMMON MANIFESTATIONS OF HEART DISEASE CHEST PAIN OTHER MANIFESTATIONS: shortness of breath palpitations weakness fatigue dizziness syncope GI complaints  PHYSICAL EXAMINATION GENERAL APPEARANCE -non-verbal behavior and body position (anxious, depressed, pain, uncomfortable) PAIN -classic sign of ischemia  PHYSICAL EXAMINATION VITAL SIGNS TEMPERATURE -note presence of fever PULSE RATE -note rate, rhythm and quality  PHYSICAL EXAMINATION VITAL SIGNS RESPIRATORY RATE -note if patient has labored breathing BLOOD PRESSURE -take BP lying, sitting, & standing positions (orthostatic VS)  CARDIAC RHYTHM -electrical activity can be observed continuously with bedside CARDIAC MONITOR -electrodes are attached to the chest & connected to a machine that displays the cardiac rhythm  HEART SOUNDS “LUB” LUB – first heart sound – referred to S1, is the closing of the mitral and tricuspid valves “DUB” DUB – referred to S2, is the closing of the aortic and pulmonic valves ABNORMAL HEART SOUNDS S3 HEART SOUND – or a ventricular gallop “LUB-DUB-DEE” LUB-DUB-DEE or “KEN-TUCK-Y” Normal in children, but indication of heart failure in an adult ABNORMAL HEART SOUNDS S4 HEART SOUND – or a atrial gallop, an extra heart sound before S1 “LUB-LUB-DUB” LUB-LUB-DUB or “TEN-NES-SEE” – - often associated with hypertensive heart disease  PERIPHERAL PULSES -palpate the radial arteries and the major arteries of the leg bilaterally -record the presence or absence of pulses and strength  SKIN -note changes in skin color (cyanosis, pallor) -note if the skin is warm or cold, dry or clammy  PERIPHERAL EDEMA EDEMA occurs when blood is not pumped efficiently or plasma protein levels are inadequate to maintain osmotic pressure AREA: feet and ankles OTHER AREAS: fingers, hands, over the sacrum Evaluated on a scale of 1-4  PERIPHERAL EDEMA PITTING EDEMA – marks of the fingers remain 1+ PITTING EDEMA – slight indentation (2mm), normal contours 2+ PITTING EDEMA – deeper pit after pressing (4mm), lasts longer than 1+  PERIPHERAL EDEMA 3+ PITTING EDEMA – deep pit (6mm), remains several seconds after pressing 4+ PITTING EDEMA – dip pit (8mm), remains prolonged time after pressing, possibly minutes  WEIGHT GAIN -can indicate edema JUGULAR VEINS -distention of this vein usually indicates increased fluid volume and pressure in the right side of the heart  MENTAL STATUS -note if patient is alert and oriented, confused and disoriented CONFUSION and DISORIENTATION can result from a decrease in the oxygen supply to the brain (cerebral ischemia) as a result of poor circulation DIAGNOSTIC TESTS LABORATORY STUDIES Enzyme, Isoenzyme, and Biochemical Markers ENZYMES CREATINE KINASE (CK) - 98% sensitivity for AMI 72 hours after infarction -present in heart muscles, skeletal muscles, and brain tissue ENZYMES CK ISOENZYMES - more specific than CK CK-MM – skeletal muscles CK-BB – appears primarily in the brain and nerve tissue CK-MB – heart muscles -generally, CK-MB levels rise 4-8hrs after the onset of AMI, peak after 20hrs, & may remain elevated for up to 72hrs ENZYMES TROPONIN I and TROPONIN T - is a protein found in the skeletal and cardiac muscles TROPONIN T – may also be found in the skeletal muscle TROPONIN I – found only in the myocardium, (more specific to myocardial damage) TROPONIN LEVELS rises within 3- 6hrs after myocardial damage. Troponin I peaks in 12-24hrs, with a return to baseline in 5-7days Troponin T peaks in 24hrs , with a return to baseline in 10-15days ENZYMES MYOGLOBIN - is a small, oxygen- binding protein found in cardiac and skeletal muscles and is rapidly released into the bloodstream ENZYMES C-REACTIVE PROTEIN (CRP) - is an inflammatory marker that may be an important risk factor for atherosclerosis and ischemic heart disease Elevated CRP is associated with AMI, stroke, and the progression of peripheral vascular disease ENZYMES LIPOPROTEIN - a molecule that is similar to low-density lipoprotein cholesterol (LDL-C) It increases cholesterol deposits in the arterial wall, enhances oxidation of LDL-C, and inhibits fibrinolysis, resulting in the formation of atherosclerotic plaque and thrombosis ENZYMES FACTOR I or FIBRINOGEN - is directly linked to increased cardiovascular risk It is involved in the coagulation cascade (converting fibrinogen to fibrin by thrombin) HEMATOLOGIC STUDIES CBC - indication of the type and number of formed elements in the blood HEMATOLOGIC STUDIES HEMATOCRIT – expresses the relationship of the formed elements in the blood to the total volume  LOWERED when blood volume increases as in CHF  RISES when blood volume is lost as in bleeding, shock and burns HEMATOLOGIC STUDIES PROTHROMBIN TIME - measures how long it takes for prothrombin to become active in clotting process PARTIAL THROMBOPLASTIN TIME - determine deficiencies in all coagulation factors except factor VII HEMATOLOGIC STUDIES ERYTHROCYTE SEDIMENTATION RATE (ESR) - indicates the extent to which RBC settle to the bottom of the test tube containing a sample of blood  ESR rises during the inflammatory processes such as rheumatic fever and MI BLOOD CHEMISTRIES SERUM CHOLESTEROL SERUM TRIGLYCERIDES  GRAPHIC RECORDING STUDIES ECG HOLTER MONITORING GRAPHIC RECORDING STUDIES ECG - graphically record electrical current generated by the heart Helps identify primary conduction abnormalities, arrhythmias, cardiac hypertrophy, pericarditis, electrolyte imbalance, and MI GRAPHIC RECORDING STUDIES EXERCISE ECG (Stress Test) - non invasive test that helps the doctor assess cardiovascular response to an increased workload Provides diagnostic information that can’t be obtained from a resting ECG GRAPHIC RECORDING STUDIES HOLTER MONITORING - records the heart’s electrical activity for 24 hours or longer as the patient performs his usual activities and experiences normal physical and emotional stress RADIOLOGY AND IMAGING Chest X-ray Myocardial Imaging RADIOLOGY AND IMAGING CHEST X-RAY - a noninvasive tool used to visualize internal structures, such as the heart, lungs, soft tissues, and bones RADIOLOGY AND IMAGING MYOCARDIAL IMAGING - with the use of radionuclides and scintillation cameras, radionuclide angiograms can be used to assess left ventricular performance RADIOLOGY AND IMAGING ECHOCARDIOGRAPHY – a noninvasive imaging technique, records the reflection of ultra-high frequency sound waves directed at the patient’s heart RADIOLOGY AND IMAGING MRI (MAGNETIC RESONANCE IMAGING)– yields high-resolution, tomographic, three dimensional images of body structures Permits visualization of valve leaflets and structures, pericardial abnormalities and processes, ventricular hypertrophy, cardiac neoplasm, infarcted tissue RADIOLOGY AND IMAGING ULTRAFAST CT SCAN – uses a scanner that takes images as fast speeds, resulting in high resolution pictures -can identify microcalcifications in the coronary arteries RADIOLOGY AND IMAGING ELECTRON BEAM COMPUTED TOMOGRAPHY – a radiologic test that produces x-rays of the coronary arteries using electron beam -can detect and quantify calcified plaque in the coronary arteries RADIONUCLIDE IMAGING TESTS CARDIAC CATHETERIZATION AND CORONARY ANGIOGRAPHY RADIONUCLIDE IMAGING TESTS CARDIAC CATHETERIZATION AND CORONARY ANGIOGRAPHY – invasive tests, use a catheter threaded through an artery or vein into the heart -to determine the size and location of a coronary lesion, evaluate ventricular function, measure heart pressures and oxygen saturation RADIONUCLIDE IMAGING TESTS CORONARY FLOW AND PERFUSION EVALUATION – used to assess blood flow through the coronary arteries, investigate myocardial anatomy and perfusion, and determine the extent of lesions RADIONUCLIDE IMAGING TESTS DSA – combines angiography with computer processing to produce high- resolution images of cardiovascular structures -provides a clear view of arterial structures RADIONUCLIDE IMAGING TESTS VENOGRAM– Insertion of a dye into the vein for the purpose of outlining an obstruction or lesion TREATMENTS DRUG THERAPY ADRENERGICS ANTIANGINALS ANTIARRHYTHMICS ANTIHYPERTENSIVES ANTILIPEMICS ANTIPLATELET AGENTS DIURETICS INOTROPHIC AGENTS THROMBOLYTICS ANALGESIC Antipyretic, Non-Steroidal Anti- inflammatory drugs, acetaminophen, acetylsalicylic acid, ibuprofen  Relieves pain, fever, and inflammation ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS Captopril, Enalapril Prevent angiotensin I from converting to angiotensin II, a potent vasoconstrictor, thereby decreasinbg peripheral vascular resistance, blocks the secretion of aldosterone from adrenal gland ANGIOTENSIN II RECEPTOR ANTAGONISTS LOSARTAN, VALSARTAN Block angiotensin II at the receptor sites, thereby decreasing peripheral vascular resistance ANTIARRHYTHMICS Lidocaine, propanolol, amiodarone Reduce automaticity, slow conduction of electrical impulses through the heart, and prolong the refractory period of myocardial cells ANTIBIOTICS Aminoglycocides (gentamycin, tobramycin), Amoxicillin, Erythromycin, penicillin, tetracycline Prevent or treat infections caused by pathogenic microorganism ANTICHOLINERGICS Atropine Block effects of vagus nerve stimulation ANTICOAGULANTS IV Heparin, oral warfarin sodium Prevent recurrence of emboli but have no effect on emboli that are already present ANTICOAGULANTS Subcutaneous – low dose heparin (5,000 units) Prophylactically prevent deep vein thrombosis, heparin activates antithrombin III ANTILIPEMIC AGENTS Cholestyramine, clofibrate, colestipol, lovastatin Lower the serum cholesterol level by binding bile salts in the bowel and forming an insoluble complex that is excreted in the stool ANTIPLATELET AGENTS Aspirin, ticlopidine Inhibit the aggregation of platelets to form a plug, platelets do not initiate thrombus formation as readily when taking antiplatelets BETA-ADRENERGIC BLOCKERS Atenolol, metoprolol, propanolol Decrease the heart rate and the force of contraction and reduce vasoconstriction by antagonizing beta- receptors in the myocardium and vasculature BETA-ADRENERGICS Beta only (dobutamine), beta or alpha plus beta – dopamine, epinephrine, metaraminol Increase myocardial contractility and heart rate, which in turn raises blood pressure, alpha plus beta-adrenergic activity CALCIUM CHANNEL BLOCKERS Nifedipine, Verapamil Inhibit calcium ions from crossing myocardial and vascular smooth muscle, thereby producing vasodilation and decreased myocardial contractility CARDIAC GLYCOSIDES Digoxin Increase the force of myocardial contractions and slow heart rate and conduction through the atrioventricular node and bundle of His CORTICOSTEROIDS Oral hydrocortisone, oral methylprednisolone, oral prednisone Strengthen the biologic membrane, which inhibits capillary permeability and prevents leakage of fluid into the injured area and development of edema DIURETICS Loop diuretics – furosemide, potassium sparing diuretic – spironolactone, thiazide diuretic Decrease blood volume, which decreases the workload of the heart OPIOD ANALGESICS Codeine, morpine, hydromorphone Release moderate to severe pain by reducing pain sensation, producing sedation, and decreasing the emotional upset often associated with pain NITRATES Isosorbide dinitrate, nitroglycerine – sublingual, topical, patch, tablet, IV Reduce myocardial oxygen demand by promoting vasodilation and by increasing oxygen supply to myocardial tissue STOOL SOFTENERS Docusate calcium, docusate sodium Decrease the surface tension of the fecal mass to allow water to penetrate into the stool; prevents the client from straining from defecation THROMBOLYTIC AGENTS Streptokinase, urokinase Dissolve thrombus or emboli in the coronary arteries VASODILATORS Hydralazine, nitroprusside sodium Decrease preload (venous dilators) and afterload (arterial dilators); act directly on blood vessels to cause dilation and decrease peripheral vascular resistance AUTONOMIC NERVOUS SYSTEM - critical to the stability of our internal environment (homeostasis) DIVISIONS: SYMPATHETIC NERVOUS SYSTEM PARASYMPATHETIC NERVOUS SYSTEM -generally function antagonistically toward each other SYMPATHETIC NERVOUS SYSTEM - regulates the expenditure of energy - Neurotransmitter are known as CATECHOLAMINES – epinephrine, norepinephrine, and dopamine - controls “fight-or-flight responses” SYMPATHETIC NERVOUS SYSTEM ENZYMES: Monoamine oxidase (MAO) & Catechol-O-methyltransferase (COMT) 4 TYPES OF RECEPTORS: alpha1, alpha2, beta1, beta2 PARASYMPATHETIC NERVOUS SYSTEM -Works to conserve body energy and is partly responsible for slowing heart rate, digesting food, and eliminating body wastes - “rest and digest” -Neurotransmitter: ACETYLCHOLINE PARASYMPATHETIC NERVOUS SYSTEM ENZYME: Acetylcholinesterase 2 TYPES OF RECEPTORS: Nicotinic, Muscarinic (both are alkaloids) ADRENERGIC FIBERS – are NERVE ENDINGS that secrete NOREPINEPHRINE CHOLINERGIC FIBERS – are NERVE ENDINGS that liberate ACETYLCHOLINE - They produce opposite responses EXAMPLE: HEART ADRENERGIC AGENTS increase the heart rate CHOLINERGIC AGENTS slow the heart rate RESPONSES TO SYMPATHETIC ACTIVATION RESPONSES TO PARASYMPATHETIC ACTIVATION CARDIAC PACING CARDIAC PACEMAKER - is an electronic device that delivers direct electrical stimulation to stimulate the myocardium to depolarize, initiating a mechanical contraction  The PACEMAKER initiates and maintains the heart rate when the heart's natural pacemaker is unable to do so  PACEMAKERS can be used to correct bradycardias, tachycardias, sick sinus syndrome, and second- and third-degree heart blocks, and for prophylaxis  Pacing may be accomplished through a permanent implantable system, a temporary system with an external pulse generator and percutaneously threaded leads, or a transcutaneous external system with electrode pads placed over the chest CARDIAC PACEMAKER INDICATIONS 1. Symptomatic bradydysrhythmias 2. Symptomatic heart block a. Mobitz II second-degree heart block b. Complete heart block c. Bifascicular and trifascicular bundle branch blocks CARDIAC PACEMAKER INDICATIONS 3. Prophylaxis a. After acute MI: dysrhythmia and conduction defects b. Before or after cardiac surgery c. During diagnostic testing CARDIAC PACEMAKER INDICATIONS 4. Tachydysrhythmias; to break rapid rhythm disturbances a. Supraventricular tachycardia b. Ventricular tachycardia CARDIAC PACEMAKER TYPES PERMANENT PACEMAKERS Used to treat chronic heart conditions; surgically placed, utilizing a local anesthetic, the leads are placed transvenously in the appropriate chamber of the heart and then anchored to the endocardium CARDIAC PACEMAKER TYPES PERMANENT PACEMAKERS The pulse generator is placed in a surgically made pocket in subcutaneous tissue under the clavicle. Once placed and programmed it can be adjusted externally as needed. CARDIAC PACEMAKER TYPES TEMPORARY PACEMAKERS are usually placed during an emergency, such as when a patient demonstrates signs of decreased CO until the temporary condition is resolved CARDIAC PACEMAKER TYPES TEMPORARY PACEMAKERS Indicated for patients with high- grade AV blocks, bradycardia, or low CO  Temporary transvenous pacer wire with external pulse generator SURGERY  CORONARY ARTERY BYPASS GRAFTING CABG circumvents an occluded coronary artery with an autogenous graft (usually a segment of saphenous vein or internal mammary artery, thereby restoring blood flow to the myocardium  Coronary artery bypass graft surgery is done primarily to alleviate anginal symptoms as well as improve survival  CORONARY ARTERY BYPASS GRAFTING CANDIDATES FOR CABG - Severe angina from atherosclerosis - CAD with high risk of MI  TRANSMYOCARDIAL REVASCULARIZATION TMR is a relatively new procedure. Can provide relief for sever angina when medical therapy fails or the patient isn’t a candidate for angioplasty or by-pass surgery Is performed through an incision on the left side of the chest  TRANSMYOCARDIAL REVASCULARIZATION POTENTIAL COMPLICATIONS: - Arrhythmias, bleeding, damage to the great vessels, valves, and coronary arteries MINIMALLY INVASIVE CORONARY ARTERY BYPASS is CABG surgery done through a left anterior small thoracotomy (LAST) a short parasternal incision, or small incisions using port access and video- assisted technology  Minimally invasive direct grafting of left internal mammary bypass graft to left anterior descending coronary artery (LAD). Surgery is performed on the beating heart. To allow suturing of the graft anastomosis to the beating heart, pharmacologic measures such as adenosine and beta- blockers are used to slow or temporarily stop the heart PORT ACCESS CARDIAC SURGERY is another minimally invasive surgical technique that uses femorofemoral bypass through a small incision with aid of videoscopes. is performed using a small anterior thoracotomy and several small “port” chest incisions  VASCULAR REPAIR may treat: - Vessels damaged by arteriosclerotic or thromboembolic disorders (such as aortic aneurysm or arterial occlusive disease), trauma, infections, or congenital defects - Vascular obstructions that severely compromise circulation  VASCULAR REPAIR may treat: - Vascular disease that doesn’t repsond to drug therapy - Life-threatening dissecting or ruptured aortic aneurysm  VASCULAR REPAIR includes aneurysm resection, grafting, embolectomy, vena caval filtering, and vein stripping  VASCULAR REPAIR TYPES: AORTIC ANEURYSM REPAIR - Removes an aneurysmal segment of the aorta VEIN STRIPPING - Removes the saphenous vein and it's branches to treat varicosities  VASCULAR REPAIR TYPES: VENA CAVAL FILTER INSERTION - Traps emboli in the vena cava, preventing them from reaching the pulmonary vessels EMBOLECTOMY - Removes an embolism from an artery  VASCULAR REPAIR TYPES: BYPASS GRAFTING - bypasses an arterial obstruction resulting from arteriosclerosis  BALLOON CATHETER TREATMENTS PERCUTANEOUS BALLOON VALVULOPLASTY PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA)  PERCUTANEOUS BALLOON VALVULOPLASTY -can be performed in the cardiac catheterization laboratory - seeks to improve valvular function by enlarging the orifice of a stenotic heart valve caused by congenital defect, calcification, rheumatic fever, or aging  PTCA -offers a nonsurgical alternative to coronary artery bypass surgery - uses a balloon-tipped catheter to dilate a coronary artery that has become narrowed because of atherosclerotic plaque -can open an occluded coronary artery without opening the chest DISEASES OF THE HEART  Thrombus A thrombus – a blood clot that can develop anywhere in the vascular system – causing the narrowing of a vessel. – blood flow can be occluded (reduced or totally blocked)  Thrombus – develop from any injury to the vessel wall endothelial cell injury draws platelets and other mediators of inflammation to the area. substances stimulate clotting and activation of the coagulation cascade. formation can occur when blood flow through a vessel is sluggish, when blood flow is irregular or erratic – during periods of irregular heartbeat or cardiac arrest Thrombus  Embolus Embolus – a substance that travels in the bloodstream from a primary site to a secondary site – becomes trapped in the vessels at the secondary site – causes blood flow obstruction. – Most emboli are blood clots (thromboemboli) usually deep leg veins  Embolus – Other sources of emboli fat – released during the break of a long bone – produced in response to any physical trauma, and amniotic fluid » which may enter maternal circulation during the intense pressure gradients generated by labor contractions. Air and displaced tumor cells also may act as emboli to obstruct flow. CORONARY ARTERY DISEASE -focal narrowing of the large and medium-sized coronary arteries - due to deposition of atheromatous plaque in the vessel wall - LIPID or FATTY Substance - FIBROUS TISSUE ARTERIOSCLEROSIS – hardening of the arteries, which results in loss of elasticity of intimal layer of the artery ATHEROSCLEROSIS – accumulated fatty plaques made of lipids in the arteries CORONARY ARTERY DISEASE RISK FACTORS - Hereditary, - Cigarette Smoking including race - HTN - Age, Gender - Elevated Serum Cholesterol Level - Diabetes Mellitus - Physical Inactivity - Obesity - fatty, fibrous plaques - occlude the coronary arteries - reduce volume of blood flow leading to myocardial ischemia Progression of atheromatous plaque from initial lesion to complex and ruptured plaque CORONARY ARTERY DISEASE SIGNS AND SYMPTOMS ANGINA – classic symptom occurs as burning, squeezing or crushing tightness in the substernal or precordial chest - may radiate to the left arm, neck, jaw or shoulder blade 4 MAJOR FORMS OF ANGINA STABLE – pain that’s predictable in frequency and duration and can be relieved with nitrates and rest UNSTABLE – increased pain that’s easily induced 4 MAJOR FORMS OF ANGINA PRINZMETAL’S or VARIANT – from unpredictable coronary artery spasm MICROVASCULAR – impairment of vasodilator reserve, which causes angina-like chest pain in a patient with normal coronary arteries CORONARY ARTERY DISEASE OTHER SIGNS AND SYMPTOMS Nausea Vomiting Weakness Diaphoresis Cool extremities CORONARY ARTERY DISEASE DIAGNOSTICS ECG – shows ischemia Exercise ECG – provoke chest pain Coronary Angiography – reveals coronary artery stenosis or obstruction, shows arteries beyond narrowing CORONARY ARTERY DISEASE DIAGNOSTICS Laboratory evaluation– to eliminate a diagnosis of MI Serum lipid studies – to detect hyperlipidemia CORONARY ARTERY DISEASE NURSING DIAGNOSIS Acute Pain Decreased Cardiac Output Anxiety CORONARY ARTERY DISEASE TREATMENT MEDICATIONS: Nitrates Antiplatelets Antilipemics Beta-adrenergic blockers Calcium channel blockers CORONARY ARTERY DISEASE NURSING MANAGEMENT Provide care during an acute anginal attack - Nitrates (SL) -stat 12-Lead ECG CORONARY ARTERY DISEASE NURSING MANAGEMENT PROMOTE PAIN RELIEF -reduce activity to a point at which pain does not occur -Position patient for comfort; Fowler's position promotes ventilation -Administer oxygen if prescribed CORONARY ARTERY DISEASE NURSING MANAGEMENT MAINTAIN CARDIAC OUTPUT -monitor vital signs, note changes in BP -note patient complaints of headache (especially with use of nitrates) -evaluate for development of heart failure CORONARY ARTERY DISEASE NURSING MANAGEMENT DECREASING ANXIETY -Rule out physiologic etiologies for increasing or new onset of anxiety -Explain to patient and family reasons for hospitalization Encourage patient to verbalize fears and concerns CORONARY ARTERY DISEASE SURGERY Obstructive lesions may necessitate CORONARY ARTERY BYPASS surgery or PTCA CORONARY ARTERY DISEASE PREVENTION Cessation of smoking Control of high BP Diet low in saturated fat, cholesterol Limit alcohol intake Physical exercise Weight control Control of diabetes mellitus  MYOCARDIAL INFARCTION refers to a dynamic process by which one or more regions of the heart experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or death to the myocardial tissue occurs MYOCARDIAL INFARCTION Obstruction in a coronary artery resulting in necrosis Due to: Atherosclerotic plaque Thrombus Embolism  MYOCARDIAL INFARCTION CLINICAL MANIFESTATIONS CHEST PAIN Typically, persistent and crushing, located substernally with radiation to the arm, neck, jaw and unrelieved by rest or nitrates  MYOCARDIAL INFARCTION CLINICAL MANIFESTATIONS CHEST PAIN Occurs without cause, primarily early morning NOT relieved by rest or nitroglycerin Lasts 30 minutes or longer  MYOCARDIAL INFARCTION CLINICAL MANIFESTATIONS Diaphoresis, cool clammy skin, facial pallor Hypertension or hypotension Bradycardia or tachycardia Premature ventricular and/or atrial beats Palpitations, severe anxiety, dyspnea  MYOCARDIAL INFARCTION CLINICAL MANIFESTATIONS Disorientation, confusion, restlessness Fainting, marked weakness Nausea, vomiting, hiccups Atypical symptoms: epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue  MYOCARDIAL INFARCTION DIAGNOSTICS ST segment is ELEVATED. T wave inversion, presence of Q wave - Elevated CK-MB, LDH and Troponin levels CBC - Elevated WBC count MYOCARDIAL INFARCTION NURSING DIAGNOSIS Acute Pain Anxiety related to chest pain, fear of death, threatening environment Decreased Cardiac Output related to impaired contractility Activity Intolerance Risk for Injury (bleeding) related to dissolution of protective clots  MYOCARDIAL INFARCTION MANAGEMENT M – Morphine sulfate O – O2 therapy N – Nitrates A – Aspirin/Adequate rest  MYOCARDIAL INFARCTION MANAGEMENT O2 – to increase oxygenation of the blood NITRATES – to relieve chestpain MORPHINE – for analgesia ASPIRIN – to inhibit platelet aggregation  MYOCARDIAL INFARCTION MANAGEMENT -Relieve pain -Stabilize heart rhythm -Revascularize the coronary artery -Reduce cardiac workload -PTCA  MYOCARDIAL INFARCTION NURSING MANAGEMENT  Administer prescribed medications – morphine, nitrates, antilipemics, thrombolytics, anticoagulants  Provide ongoing assessment -monitor cardiac enzymes  MYOCARDIAL INFARCTION NURSING MANAGEMENT  Minimize anxiety  Minimize metabolic demands -institute a liquid diet, advance to a low sodium, low cholesterol, low fat diet  MYOCARDIAL INFARCTION NURSING MANAGEMENT  prepare the client for treatment, such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting  HEART FAILURE  is a syndrome of pulmonary or systemic circulatory congestion caused by decreased myocardial contractility, resulting in inadequate CO to meet oxygen requirements of tissues.  HEART FAILURE CLASSIFICATION: LEFT-SIDED (or left ventricular) RIGHT-SIDED (or right ventricular)  HEART FAILURE LEFT-SIDED - congestion occurs primarily in the lungs from backup of blood into pulmonary veins and capillaries because of left ventricular pump failure. As blood backs up into the pulmonary bed, increased hydrostatic pressure causes fluid accumulation in the lungs. Blood flow is consequently decreased to the brain, kidneys, and other tissues  HEART FAILURE RIGHT-SIDED - congestion in systemic circulation results from right ventricular pump failure. As blood backs up into the pulmonary bed, increased hydrostatic pressure produces peripheral and dependent pitting edema. Venous congestion in the kidneys, liver, and GI tract also develops.  HEART FAILURE CAUSES: -atherosclerotic heart disease -MI -hypertension -Rheumatic heart disease -congenital heart disease -ischemic heart disease -Arrhythmias  HEART FAILURE DIAGNOSTICS: ECHOCARDIOGRAPHY - depressed cardiac output, evidence of cardiomegaly CHEST X-RAY-reveals cardiomegaly ABG-decreased partial pressure of arterial O2  HEART FAILURE CLINICAL MANIFESTATIONS LEFT SIDED HEART FAILURE -dyspnea on exertion, paroxysmal nocturnal dyspnea, or orthopnea -crackles on lung auscultation -frothy blood-tinged sputum -tachycardia with S3 heart sound -pale, cool extremities -peripheral and central cyanosis  HEART FAILURE CLINICAL MANIFESTATIONS LEFT SIDED HEART FAILURE -decreased peripheral pulses and capillary refill Decreased urinary output easy fatigability Insomnia and restlessness  HEART FAILURE CLINICAL MANIFESTATIONS RIGHT SIDED HEART FAILURE dependent pitting edema (peripheral and sacral) Weight gain Nausea and anorexia Jugular vein distention Liver congestion, ascites, weakness  HEART FAILURE NURSING DIAGNOSIS: Decreased CO related to an ineffective ventricular pump  HEART FAILURE PHARMACOLOGIC TREATMENT: Vasodilators Diuretics Digoxin Dobutamine Beta-adrenergic blocking agents (metoprolol, carvedilol)  HEART FAILURE NURSING MANAGEMENT:  Administer medications as ordered  Provide ongoing assessment -Monitor hemodynamic parameters, HR, rhythm, -weigh OD  Prevent complications of immobility  HEART FAILURE NURSING MANAGEMENT:  Provide a low-sodium diet, as prescribed  provide client and family teaching  HYPERTENSION  refers to an intermittent or sustained elevation in diastolic or systolic blood pressure  HYPERTENSION TYPES: ESSENTIAL (IDIOPATHIC) – most common form SECONDARY – results from a number of disorders that impair blood pressure regulation MALIGNANT HYPERTENSION – severe, fulminant form of hypertension common to both types  HYPERTENSION CAUSES: ESSENTIAL (IDIOPATHIC) –associated with risk factors such as genetic predisposition, stress, obesity, and a high-sodium diet  HYPERTENSION CAUSES: SECONDARY – results from underlying disorders that impair blood pressure regulation, particularly renal, endocrine, vascular, and neurological disorders; hypertensive disease of pregnancy (formerly known as toxemia); and use of estrogen-containing oral contraceptives  HYPERTENSION CAUSES: MALIGNANT HYPERTENSION – not known, but it may be associated with dilation of cerebral arteries and generalized arteriolar fibrinoid necrosis, which increases intracerebral blood flow, resulting in encephalopathy  Guidelines for Determining Hypertension Category Systolic Pressure Diastolic Pressure Normal 100 mm Hg hypertension  HYPERTENSION RISK FACTORS Family history of hypertension Race (more common in blacks) Gender Diabetes mellitus Stress Obesity  HYPERTENSION RISK FACTORS High dietary intake of saturated fats or sodium Tobacco use Hormonal contraceptive use Sedentary lifestyle aging  HYPERTENSION SYMPTOMS: blood pressure measurements of more than 140/90mmHg Throbbing occipital headaches upon waking Drowsiness Confusion vision problems nausea  HYPERTENSION DIAGNOSTICS: BUN - May be elevated SERUM CREATININE - determines if renal dysfunction is present as a complication of hypertension Total cholesterol, Triglycerides Electrocardiogram  HYPERTENSION TREATMENT: SECONDARY HPN - correcting the underlying cause and controlling hypertensive effects LIFESTYLE MODIFICATIONS: change in diet, relaxation techniques, exercise, smoking cessation, limited intake of alcohol  HYPERTENSION TREATMENT: DRUG THERAPY THIAZIDE – for uncomplicated HPN ACE INHIBITOR BETA-ADRENERGIC BLOCKER  HYPERTENSION TREATMENT: DRUG THERAPY Angiotensin II receptor blockers Alpha-receptor blockers Calcium channel blockers  HYPERTENSION NURSING DIAGNOSIS: Knowledge deficit related to chronic disease management INTERVENTIONS: Health education; Teaching: Diet, Disease process, Health behaviors, Medication, Prescribed activity, Treatment regimen  INFLAMMATORY DISORDERS OF THE PERIPHERAL BLOOD VESSELS  VARICOSE VEINS Permanently distended veins that develop from loss of valvular competency Faulty valves elevate venous pressure Causes distension and tortuosity  Predisposing Factors Pregnancy Obesity Heart disease  Assessment Findings Aching, a feeling of heaviness in the legs Itching, moderate swelling Superficial inflammation Dilated tortuous skin veins  Diagnostic test Trendelenberg test: Doppler ultrasound – Decrease or no blood flow heard after calf or thigh compression Medical Management  THROMBOPHLEBITIS -is an inflammation of a vein accompanied by clot or thrombus formation DEEP VEIN THROMBOSIS – veins that are deep in the lower extremeties  THROMBOPHLEBITIS -when inner lining of a vein is irritated or injured, platelets clump together, forming a clot  Clot interferes with blood flow, causing congestion of venous blood  THROMBOPHLEBITIS SIGNS AND SYMPTOMS -complaints of discomfort in the affected extremity -Calf pain (+Homan’s sign) -heat, redness, swelling on the affected vein  THROMBOPHLEBITIS DIAGNOSTICS VENOGRAPHY – indicates a filling defect in the area of the clot  THROMBOPHLEBITIS MANAGEMENT Complete rest of the affected part anticoagulant therapy (heparin) Continues warm, wet packs – to improve circulation, ease pain, decrease inflammation THROMBECTOMY- surgical removal of the clot THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)  Inflammatory, nonatheromatous occlusive condition that causes segmental lesions and subsequent thrombus formation - affects small arteries and veins of the legs THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE) CAUSE: -unknown but definite link to smoking CLINICAL MANIFESTATIONS: -Intermittent Claudication THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE) - No specific treatment exist, except smoking cessation - Amputation maybe necessary for patients with gangrene formation  INFECTIOUS AND INFLAMMATORY DISORDERS OF THE HEART  RHEUMATIC FEVER is a systemic inflammatory disease that sometimes follows a group A streptococcal infection of the throat RHEUMATIC CARDITIS refers to the inflammatory cardiac manifestations of Rheumatic Fever in either the acute or later stage  RHEUMATIC FEVER STRUCTURES AFFECTED: heart valves, praticularly mitral valve endocardium myocardium pericardium  RHEUMATIC FEVER STREPTOCOCCAL INFECTION  Antistreptococcal antibodies attack normal heart cells     Rheumatic carditis develops  RHEUMATIC FEVER SIGNS AND SYMPTOMS: most common in children 2-3 weeks after a streptococcal infection CARDITIS – inflammation of the layers of the heart  RHEUMATIC FEVER POLYARTHRITIS – inflammation of more than 1 joint rash, subcutaneous nodules, chorea (characterized by involuntary grimacing & an inability to use skeletal muscles in coordinated manner  RHEUMATIC FEVER SIGNS AND SYMPTOMS: mild fever Heart rate (rapid, rhythm abnormal) Red, spotty rash (trunk, disappears rapidly) Swollen, warm, red & painful joints  RHEUMATIC FEVER DIAGNOSTICS: no specific laboratory tests ASO titer ESR, C-reactive protein – elevated, ECG, ECHOCARDIOGRAPHY – structural changes in the heart  RHEUMATIC FEVER MEDICAL MANAGEMENT: IV ANTIBIOTICS: PENICILLIN – drug of choice Others: AZYTHROMYCIN (ZYTHROMAX), CLINDAMYCIN, VANCOMYCIN CEPHALOSPORINS: Cephalexin, Cefadroxil  RHEUMATIC FEVER MEDICAL MANAGEMENT: ASPIRIN – to control the formation of blood clots around heart valves STEROIDS – to suppress the inflammatory response BED REST  RHEUMATIC FEVER MEDICAL MANAGEMENT: SURGERY may be required to treat constrictive pericarditis and damage to heart valves  RHEUMATIC FEVER NURSING MANAGEMENT:  Administer prescribed drug therapy and monitor for therapeutic and adverse effects  Plan diversional activities that require minimal activity INFECTIVE ENDOCARDITIS formerly called BACTERIAL ENDOCARDITIS  is inflammation of the inner layer of heart tissue as a result of an infectious microorganism MICROORGANISM – bacteria and fungi BACTERIA: Streptococcus viridans, Staphylococcus aureus  INFECTIVE ENDOCARDITIS SIGNS AND SYMPTOMS: -can have an acute onset – less than one week -fever, chills, muscle aches in the lower back and thighs, joint pain ADVANCE: OSLER NODES - purplish, painful nodules, appear on the pads of the fingers & toes  INFECTIVE ENDOCARDITIS SIGNS AND SYMPTOMS: -SPLINTER HEMORRHAGES – black longitudinal lines can be seen in the nails -JANEWAY LESIONS – small, painless, red-blue macular lesions on the palms and soles of the feet INFECTIVE ENDOCARDITIS SIGNS AND SYMPTOMS: -ROTH’S SPOT – white areas in the retina surrounded by areas of hemorrhage -HEART MURMUR – may be present from malfunctioning valves INFECTIVE ENDOCARDITIS SIGNS AND SYMPTOMS: -PETECHIAE – tiny red-dish hemorrhagic spots on the skin and mucous membranes -weakness, anorexia, weight loss INFECTIVE ENDOCARDITIS DIAGNOSTICS -BLOOD CULTURE – to determine microorganism circulating in the blood -ECG INFECTIVE ENDOCARDITIS MEDICAL MANAGEMENT High doses of IV Antibiotics Antibiotic Therapy extends at least 2- 6 weeks Bed rest SURGERY – valve replacement if heart valve is severely damaged INFECTIVE ENDOCARDITIS NURSING MANAGEMENT Remind client to limit activity Assess for changes in weight and pulse rate and rhythm Administer prescribed antibiotics Inform client that periodic antibiotic therapy is a lifelong necessity because they will be vulnerable to the disease for the rest of their lives  MYOCARDITIS is an inflammation of the myocardium (the muscle layer of the heart) CAUSES: Viral, bacterial, fungal, or parasitic infections VIRAL AGENTS: coxsackie virus A & B, influenza A & B, measles, adenovirus, mumps, rubeola, rubella  MYOCARDITIS Inflammatory response causes the cardiac muscle to swell  Interferes with the myocardium’s ability to stretch and recoil  Cardiac output is reduced and blood circulation is impaired, predisposing the client to CHF  MYOCARDITIS CLINICAL MANIFESTATIONS: -sharp stabbing pain or squeezing chest discomfort that resembles a MI (pain is relieved by sitting up) -Low-grade fever, tachycardia, dysrhythmias -Dyspnea, malaise, fatigue, anorexia -Skin is pale and cyanotic  MYOCARDITIS CLINICAL MANIFESTATIONS: IF THERE’S IMPAIRED HEART’S PUMPING ACTIVITY: -Neck vein distention, ascites, -Peripheral edema, -crackles  MYOCARDITIS DIAGNOSTICS: -WBC – elevated -C-Reactive protein – elevated, inflammatory conditions -CARDIAC ISOENZYMES-elevated -CHEST X-RAY – heart enlargement, fluid infiltration in the lungs  MYOCARDITIS MANAGEMENT Treat underlying cause and prevent complications ANTIBIOTICS if bacterial Bed Rest Sodium-restricted diet Cardiotonic drugs – digitalis to prevent or treat heart failure  MYOCARDITIS MANAGEMENT Heart transplant is necessary in severe cases of cardiomyopathy  MYOCARDITIS NURSING MANAGEMENT Monitor client’s cardiopulmonary status (daily weights, vital signs, I & O, heart & lung sounds, edema) Maintain bed rest Administer antipyretics if patient has fever Elevate head of the bed for maximal breathing potential  CARDIOMYOPATHY is a chronic condition characterized by structural changes in the heart muscle TYPES: DILATED CARDIOMYOPATHY HYPERTROPHIC CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY  CARDIOMYOPATHY DILATED CARDIOMYOPATHY -dyspnea on exertion & when lying down, fatigue, edema, palpitations, chestpain HYPERTROPHIC CARDIOMYOPATHY -syncope, fatigue, shortness of breath, chestpain -some are asymptomatic  CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY -exertional dyspnea, dependent edema in the legs, ascites, hepatomegaly  CARDIOMYOPATHY DILATED CARDIOMYOPATHY -the cavity of the heart is stretched (dilated) CAUSES: Viral myocarditis, Autoimmune response, chemicals (chronic alcohol ingestion) TREATMENT: Drug Therapy to minimize symptoms & prevent complications, abstinence from alcohol, salt restriction, weight loss, possible heart transplantation  CARDIOMYOPATHY HYPERTROPHIC CARDIOMYOPATHY -the muscle of the left ventricle & septum thickens, causing heart enlargement) CAUSES: hereditary, unknown TREATMENT: Drug Therapy to reduce heart rate & force of contraction, antidysrhythmic drugs, artificial pacemaker  CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY -heart muscle stiffens, which interferes with its ability to stretch & fill with blood CAUSES: deposits of amyloid, scleroderma, TREATMENT: no specific treatment, drugs such as diuretics & antihypertensives used to control symptoms  CARDIOMYOPATHY TREATMENT: -DIURETICS -CARDIAC GLYCOSIDES -ANTIHYPERTENSIVE  PERICARDITIS inflammation of the pericardium PRIMARY – develops independently of any other condition SECONDARY – develops because of another condition  PERICARDITIS Usually secondary to endocarditis, myocarditis, chest trauma or MI OTHER CAUSES: tuberculosis, malignant tumors, uremia  PERICARDITIS SIGNS AND SYMPTOMS Fever and malaise Dyspnea, or complaints of chest heaviness PRECORDIAL PAIN (relieved by upright or leaning forward)  PERICARDITIS DIAGNOSTICS ECG – ST segment elevation (cardiac isoenzymes normal) ECHOCARDIOGRAPHY WBC & ESR - elevated  PERICARDITIS MANAGEMENT Rest DRUGS: Analgesics, antipyretics, NSAIDs, corticosteroids PERICARDIOCENTESIS – needle aspiration of fluid from between the visceral and parietal pericardium