MEDSURG_WEEK 1 & 2 PDF - Medical Surgical

NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - WK1:CU1-- DISTURBANCES IN PUMPING MECHANISM INFLAMMATORY DISORDERS AND HEART FAILURE The...

NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - WK1:CU1-- DISTURBANCES IN PUMPING MECHANISM INFLAMMATORY DISORDERS AND HEART FAILURE The heart lies in a rotated position within the chest cavity. ANATOMY OF THE HEART The right ventricle lies anteriorly (just beneath the sternum) and the left ventricle is situated posteriorly. HEART a hollow, muscular organ apical impulse/point of maximal impulse location: center of the thorax close proximity to the chest wall, the pulsation created during occupies the space between the lungs normal ventricular contraction, called PMI, is easily detected. (mediastinum) and rests on the diaphragm. located at the intersection of the midclavicular line of the left chest weight: approx 300 g (10.6 oz) wall and the fifth intercostal space. pumps blood to the tissues, supplying them with oxygen and other nutrients. Heart Valves four valves 3 layers of the heart permit blood to flow in only one direction. thin leaflets of fibrous tissue 1. endocardium open and close in response to the movement of blood and inner layer pressure changes within the chambers. endothelial tissue two types of valves: inside of the heart and valves 2. Myocardium 1. Atrioventricular Valves middle layer separate the atria from the ventricles. muscle fibers pumping action a. tricuspid valve three cusps or leaflets separates the right atrium from the right ventricle. 3. Epicardium exterior layer of the heart b. mitral or bicuspid valve two cusps PERICARDIUM lies between the left atrium and the left ventricle two layers encased the heart with a thin, fibrous sac 2. Semilunar Valves visceral pericardium three leaflets Adhering to the epicardium shaped like half-moon closed during diastole parietal pericardium pressure in the pulmonary artery and aorta decreases, Enveloping the visceral pericardium causing blood to flow back toward the semilunar valves. a tough fibrous tissue a. Pulmonic valve supports the heart in the mediastinum. b/w the right ventricle and the pulmonary artery pericardial space b. Aortic valve space between these two layers filled with 20 mL of fluid The valve between the left ventricle and the aorta lubricates the surface of the heart reduces friction during systole. Coronary Arteries Heart Chambers left and right coronary arteries 4 chambers supply arterial blood to the heart rhythmic relaxation and contraction of the originate from the aorta just above the aortic valve muscular walls ==> pumping action of the leaflets heart Left coronary artery diastole has three branches relaxation phase four chambers relax 1. left main coronary artery period of ventricular filling --> preparing for from the point of origin to the first major branch contraction 2. left anterior descending artery from the left main coronary artery courses down the anterior wall Systole of the heart events in the heart during contraction of the two top chambers (atria) and two bottom 3. circumflex artery chambers (ventricles). from the left main coronary artery circles around to the lateral left wall of the heart NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Right Coronary artery Cardiac Cycle The posterior wall of the heart receives its blood supply by an additional branch from the right composed of both systole and diastole. coronary artery called the posterior descending occur from one heartbeat to the next. artery cause blood to flow through the heart Superficial to the coronary arteries are the coronary veins. Cardiac Output Venous blood from these veins returns to the heart primarily through the coronary sinus, which is amount of blood pumped by each ventricle during a located posteriorly in the right atrium. given period. normal resting adult = 5 L/min Myocardium computed by multiplying the stroke volume by the the middle, muscular layer of the atrial and heart rate. ventricular walls. composed of specialized cells called myocytes, which Stroke volume form an interconnected network of muscle fibers. amount of blood ejected per heartbeat. These fibers encircle the heart in a figure-of eight resting stroke volume = 70mL pattern, forming a spiral from the base (top) of the heart to the apex (bottom). Control of Heart Rate During contraction, this muscular configuration Cardiac output must be responsive to changes in the facilitates a twisting and compressive movement of metabolic demands of the tissues. the heart that begins in the atria and moves to the ventricles. the heart rate is affected by central nervous system and Function of the Heart baroreceptor activity. Cardiac Electrophysiology Baroreceptors specialized nerve cells generates and transmits electrical impulses that located in the aortic arch and in both right and left stimulate contraction of the myocardium. internal carotid arteries first stimulates contraction of the atria and then sensitive to changes in blood pressure (BP) the ventricles. During hypertension Three physiologic characteristics of the nodal barorecepetor cells cells and the Purkinje cells transmitting impulses to the cerebral medulla. (two types of specialized electrical cells) initiates parasympathetic activity lowering the heart rate and the BP 1. Automaticity: initiate an electrical impulse 2. Excitability: arespond to an electrical impulse During hypotension 3. Conductivity: transmit an electrical impulse from baroreceptor stimulation one cell to another decrease in parasympathetic inhibitory activity vasoconstriction and increased heart rate elevate the Both the sinoatrial (SA) node and the BP. atrioventricular (AV) node are composed of nodal cells. Control of Stroke Volume Stroke volume is primarily determined by three SA node factors: preload, afterload, and contractility. primary pacemaker of the heart located at the junction of the superior vena cava 1. Preload and the right atrium degree of stretch of the ventricular cardiac muscle normal resting adult heart = 60 to 100 impulses fibers at the end of diastole. per minute The end of diastole is the period when filling volume in the ventricles is the highest and the degree of stretch on the muscle fibers is the greatest. left ventricular end-diastolic pressure (LVEDP) The volume of blood within the ventricle at the end of diastole determines preload, which directly affects stroke volume. Frank-Starling (or Starling) law of the heart volume of blood returning to the heart muscle fiber stretch = increased preload result = stronger contraction and a greater stroke volume. NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - To reduce preload Diuretics ASSESSMENT OF CARDIOVASCULAR venodilating agents (eg, nitrates) excessive loss of blood, or dehydration (excessive SYSTEM loss of body fluids from vomiting, diarrhea, or diaphoresis) 1. Common symptoms (chest pain or discomport, shortness of breath, peripheral edema, weight gain, Preload is increased by increasing the return of palpitations, vital fatigue, dizziness) circulating blood volume to the ventricles. 2. Chest pain 3. Past Health, Family, and Social History ways to increase preload 4. Medications Controlling the loss of blood or body fluids and 5. Nutrition replacing fluids (ie, blood transfusions and 6. Elimination (Nocturia-- common in HF) intravenous [IV] fluid administration). 7. Activity and Exercise 8. Blood Pressure 2. Afterload 9. Pulse pressure resistance to ejection of blood from the ventricle 10. Arterial pulses second determinant of stroke volume. 11. Pulse rate 12. Pulse rhythm systemic vascular resistance 13. Pulse quality The resistance of the systemic BP to left 14. Heart inspection and palpation (aortic, pulmonic, erb's ventricular ejection. point, tricuspid, mitral, epigastric) 15. Heart auscultation 16. Normal heart sounds (S1, S2) pulmonary vascular resistance 17. Abnormal heart sounds (S3, S4) The resistance of the pulmonary BP to right 18. Murmurs ventricular ejection. 19. Friction rub (harsh, grating sound) 3. Contractility Other organs: force generated by the contracting myocardium. Lungs 1. Hemoptysis ejection fraction 2. Cough The percentage of the end-diastolic blood volume 3. Crackles that is ejected with each heartbeat. 4. Wheezes The ejection fraction of the normal left ventricle is 55% to 65%. Abdomen The right ventricular ejection fraction is rarely 1. Abdominal distention measured. 2. Hepatojugular reflux The ejection fraction is used as a measure of 3. Bladder distention myocardial contractility. An ejection fraction of less than 40% = tpatient has decreased left ventricular function DIAGNOSTIC EVALUATION = requires treatment for heart failure (HF) 1. Cardiac Biomarker Analysis (12 Lead ECG) 2. Blood chemistry, hematology, coagulation studies (Lipid, cholesterol, triglycerides) 3. Brain (B Type) Natriuretic Peptide (regulate BP and fluids) 4. C reactive protein (CVD, inflammation) 5. Homocysteine (CVD, CAD, atherosclerosis) 6. Chest X-ray and Fluoroscopy (image) 7. ECG (heart electrical currents) 8. Telemetry -- wireless ecg 9. Ambulatory ECG -- outpatient settings 10. Cardiac stress testing (exercise and pharmacologic) 11. Traditional ECG -- noninvasive (pericardial effusions) 12. Transesophageal ECG 13. Magnetic Resonance Angiography 14. Cardiac catheterization 15. Angiography 16. Central venous pressure monitoring 17. Pulmonary artery pressure monitoring NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Electrocardiogram PR interval The electrical impulse that from the beginning of the travels through the heart P wave to the beginning can be viewed by means of of the QRS complex electrocardiography the time needed for sinus end product = node stimulation, atrial electrocardiogram (ECG) depolarization, and Each phase of the cardiac conduction through the A cycle is reflected by specific V node before ventricular waveforms on the screen of depolarization. a cardiac monitor or on a strip of ECG graph paper. ST segment early ventricular repolarization waveforms from the end of the QRS P wave complex to the beginning QRS complex of the T wave. T wave U wave QT interval 1-minute rhythm strip total time for ventricular contains 300 large boxes and 1500 small depolarization and boxes. segments and intervals repolarization PR interval from the beginning of the easy and accurate method of determining ST segment QRS complex to the end heart rate with a regular rhythm is to count QT interval of the T wave. the number of small boxes within an RR interval and divide 1500 by that number. P wave TP interval electrical impulse starting in from the end of the T example the SA node and spreading wave to the beginning of there are 10 small boxes through the atria. the next P wave between two R waves atrial depolarization. preferred reference for heart rate is 1500/10 = 150 bpm the isoelectric line. QRS complex there are 25 small boxes ventricular depolarization. PP interval heart rate is 1500/25 = 60 bpm Not all QRS complexes have from the beginning of all three waveforms. one P wave to the first negative deflection beginning of the next P after the P wave. wave. determine atrial rate and T wave rhythm. ventricular repolarization when the cells regain a RR interval negative charge - resting from one QRS complex state) to the next QRS complex. follows the QRS complex determine ventricular Large square and is usually the same rate and rhythm = 300/RR interval direction (deflection) as the QRS complex. Small square = 1500/ RR interval U wave repolarization of the Purkinje fibers follows the T wave and is usually smaller than the P wave this wave is rare patients with hypokalemia (low potassium levels), hypertension, or heart disease.  ⬆⬆ NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Inflammatory/Infectious Disorders of the Heart 1. PERICARDITIS Clinical manifestation (cardiac tamponade) 2. INFECTIVE chest pain ENDOCARDITIS creaky or scratchy friction rub 3. MYOCARDITIS mild fever 4. HEART FAILURE WBC count, anemia, and an ESR or C- RP nonproductive cough or hiccup 1. Pericarditis (Cardiac Tamponade) Dyspnea inflammation of the pericardium heart rate Chest pain (most common sx) May be acute, chronic, or recurrent Clinical Manifestations of Cardiac Can be infectious or non infectious Tamponade may occur after pericardiectomy (opening of the Falling blood pressure pericardium) following cardiac surgery rising venous pressure (distended neck may occur 10 days to 2 months after acute myocardial veins) infarction (Dressler syndrome). distant (muffled) heart sounds with pulsus Pagthophysiology paradoxus inflammatory process of pericarditis Assessment Findings = accumulation of fluid in the pericardial sac (pericardial effusion) history, signs, and symptoms. = pressure on the heart = cardiac tamponade Diagnostic Findings Frequent or prolonged episodes of pericarditis = thickening and elasticity of the pericardium, = 1. echocardiogram scarring may fuse the visceral and parietal inflammation, pericardial effusion or pericardium. tamponade, and heart failure. restrict the heart’s ability to fill with blood guide pericardiocentesis (constrictive pericarditis). The pericardium may become calcified, further 2. CT imaging restricting ventricular expansion during ventricular best diagnostic tool for determining size, filling (diastole). shape, and location of pericardial effusions With less filling, the ventricles pump less blood, used to guide pericardiocentesis. = cardiac output and signs and symptoms of heart 3. Cardiac MRI failure. Restricted diastolic filling assist with detection of inflammation and adhesions. = systemic venous pressure --> peripheral edema and hepatic failure. 4. video-assisted pericardioscope-guided biopsy obtain tissue samples for culture and microscopic examination. Causes idiopathic 5. 12-lead ECG infection (usually viral, rarely bacterial or fungal) concave ST elevations autoimmune disorders depressed PR segments or atrial arrhythmia connective tissue disorders Immune-mediated drug reactions hypersensitivity states constrictive pericarditis diseases of adjacent structures Frequent or prolonged episodes of neoplastic disease pericarditis = thickening and decreased radiation therapy elasticity that restrict the heart’s ability to fill chest trauma properly with blood renal disorders tuberculosis (TB) pericardial e!usion The pericardium may also become calcified, Pericarditis may be subacute, acute, or chronic and may which restricts ventricular contraction. be classified by the layers of the pericardium becoming Pericarditis can lead to an accumulation of attached to each other (adhesive) or by what accumulates fluid in the pericardial sac (pericardial in the pericardial sac: effusion) and increased pressure on the serum (serous) heart, leading to cardiac tamponade. pus (purulent) calcium deposits (calcific) clotting proteins (fibrinous) blood (sanguinous). NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Medical Management 1. bed rest until fever, chest pain, and friction rub have subsided When cardiac output is impaired 2. Analgesic medications and NSAIDs aspirin, indomethacin, or ibuprofen 3. Corticosteroids (e.g., prednisone) alternative when NSAIDs are contraindicated (e.g., kidney disease). 4. Colchicine if pericarditis is severe as an additive therapy to NSAIDs 5. Pericardiocentesis some pericardial fluid is removed to assist in identification of the cause 6. pericardial window small opening made in the pericardium allow continuous drainage into the chest cavity. 7. pericardiectomy Surgical removal of tough encasing pericardium release both ventricles from constrictive and restrictive inflammation and scarring. Nursing Management pain management with antispasmodic agents, assistance with positioning, and psychological support. education and reassurance that the pain is not due to a heart attack. Pain may be relieved with a forward-leaning or sitting position. activity restrictions until pain and fever subside. encourages gradual increases of activity. healthy lifestyle to enhance the patient's immune system. must be alert to signs and symptoms of cardiac tamponade monitors the patient for heart failure. NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - 2. INFECTIVE ENDOCARDITIS microbial infection of the endothelial surface of Clinical Manifestations the heart. fever and a heart murmur (primary sx) malaise, anorexia, weight loss, cough, and back and usually develops in joint pain. > older adults Small, painful nodules (Osler nodes) --> pads of fingers > people with prosthetic heart valves or toes. > or with cardiac devices. Irregular, red or purple, painless, flat macules (Janeway lesions) --> palms, fingers, hands, soles, and Staphylococcal endocarditis infections of valves in toes the right side of the heart are common among adults Hemorrhages with pale centers (Roth spots) caused by who use illicit IV drugs emboli may be observed in the fundi of the eyes. Splinter hemorrhages --> under the fingernails and Hospital-acquired infective endocarditis occurs most toenails. often Petechiae --> conjunctiva and mucous membranes. in patients with debilitating disease or indwelling Cardiomegaly, heart failure, tachycardia, or catheters splenomegaly may occur. in patients who are receiving hemodialysis or headache, temporary or transient cerebral ischemia, prolonged IV fluid or antibiotic therapy and strokes Embolization Pathophysiology Assessment and Diagnostic Findings deformity or injury of the endocardium 1. Two separate blood culture definitive leads to accumulation of fibrin and platelets (clot formation) on the endocardium. 2. Echocardiogrm Heart vegetation Infectious organisms, usually staphylococci or streptococci, invade the clot and endocardial lesion. 3. white blood cell Infection most frequently results in platelets, fibrin, 4. Echocardiography blood cells, and microorganisms that cluster as mass on a valve, prosthetic valve, or supporting vegetations on the endocardium. structures by identifying vegetations, abscesses, new prosthetic Vegetations may embolize to other vessels valve dehiscence, or new regurgitation. throughout the body. Prevention Antibiotic prophylaxis (penicillin) -- w/ allergy = As the clot on the endocardium continues to expand, amoxicillin or clindamycin the infecting organism is covered by new clot and Advise not to use IUD concealed from the body's normal defenses. Poor dental hygiene --> lead to bacteremia, particularly in the setting of a dental procedure. Infection may erode through the endocardium into Increased vigilance --> px with IV catheters and during underlying structures (e.g., valve leaflets), causing invasive procedures. tears or other deformities of valve leaflets, dehiscence meticulous hand hygiene, site preparation, and aseptic of prosthetic valves, deformity of chordae tendineae, technique during insertion and maintenance or mural abscesses. procedures. Risk factors Medical Management Prosthetic cardiac valves or prosthetic material to eradicate invading organisms through adequate used for cardiac valve repair doses of an appropriate antibiotic. Implanted cardiac devices (e.g., pacemaker, implanted cardioverter defibrillator) Blood culture History of bacterial endocarditis (even without Monitor Temp heart disease) Congenital heart disease Antibiotic therapy IV Cardiac transplant recipients with valvulopathy 2 to 6 weeks. IV drug abuse Body piercing (especially oral, nasal, and nipple), Parenteral therapy branding, and tattooing high serum concentration Hemodialysis eradication of the dormant bacteria within dense Hospital-acquired endocarditis vegetations. immunosuppressive medications delivered in the patient’s home monitored by a home health nurse NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Surgical Management Reason heart failure intracardiac abscess recurrent systemic embolizations infection does not respond to medications. 1. valve repair and replacement 2. débridement of vegetations 3. débridement and closure of an abscess 4. closure of a fistula 5. Surgical valve replacement greatly Prosthetic valve endocarditis require repeat valve replacement Nursing Management monitors temperature at regular intervals --> indication of treatment effectiveness. administers antibiotic, antifungal, or antiviral medication Timing of antimicrobial medication administration is critical rest periods and provide rest between activities. Good infection control and prevention Nonsteroidal anti-inflammatory drugs (NSAIDs) may be prescribed as antipyretics or to decrease the discomfort of fever. Heart sounds are assessed. murmur --> dehiscence of a prosthetic valve, rupture of an abscess, or injury to valve leaflets or chordae tendineae monitors for signs and symptoms of systemic embolization, or, for patients with right- sided heart endocarditis, for signs and symptoms of pulmonary infarction and infiltrates. assesses signs and symptoms of organ damage such as stroke, meningitis, heart failure, myocardial infarction, glomerulonephritis, and splenomegaly. All invasive lines and wounds must be assessed daily for redness, tenderness, warmth, swelling, drainage, or other signs of infection. The patient and family are educated about activity restrictions, medications, and signs and symptoms of infection. Patients with infective endocarditis are at high risk for another episode of infective endocarditis. NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - 3. MYOCARDITIS Assessment and Diagnostic Findings inflammatory process involving the myocardium. may reveal no detectable abnormalities may be tachycardic --> can cause may report chest pain heart dilation thrombi on the heart wall (mural thrombi) Px w/o abnormal heart structure infiltration of circulating blood cells around the coronary vessels and between the muscle develop arrhythmias fibers ST–T-wave changes. degeneration of the muscle fibers themselves Px has heart abnormalities --> results from an infectious process disclose cardiac enlargement viral bacterial faint heart sounds (especially S1) rickettsial fungal pericardial friction rub parasitic metazoal gallop rhythm protozoal spirochetal systolic murmur. endomyocardial biopsy --> may develop in patients receiving immunosuppressive therapy definitive diagnosis with infective endocarditis Crohn disease cardiac MRI systemic lupus erythematosus used more often noninvasive approach Pathophysiology guide for endomyocardial biopsies results from: 1. infectious source (viral, bacterial, rickettsial, Elevated fungal, parasitic, metazoal, protozoal, WBC count C-reactive protein spirochetal) leukocyte count ESR 2. immune related, occurring after acute systemic infections such as rheumatic fever, or it may be related to an autoimmune Medical Management disorder. 3. inflammatory reaction to toxins such as 1. bed rest pharmacologic agents used in the treatment cardiac workload of other diseases myocardial damage complications of myocarditis. begin in one small area of the myocardium spread throughout the myocardium 2. Limit Activties degree of myocardial inflammation = degree young patients --> limited for a 6-month period of interstitial collagen and elastin destruction or at least until heart size and function have The greater the destruction, the greater is the returned to normal. hemodynamic effect and resulting signs and symptoms. 3. NSAIDs DCM and HCM are latent manifestations of should not be used for pain control myocarditis. cardiac injury and viral replication in animal Clinical Manifestations studies fatigue dyspnea Nursing Management Syncope resolution of tachycardia, fever, and any other palpitations clinical manifestations. occasional discomfort in the chest and upper cardiovascular assessment focuses on signs and abdomen symptoms of heart failure and arrhythmias. flulike = most common Patients with arrhythmias should have sustain sudden cardiac death continuous cardiac monitoring with personnel quickly develop severe congestive heart and equipment readily available to treat life- failure in fulminant myocarditis threatening arrhythmias NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - 4. Heart Failure congestive HF Atherosclerosis inability of the heart to pump sufficient blood to meet the primary cause of HF needs of the tissues for oxygen and nutrients. characterized by fluid overload or inadequate tissue perfusion. CAD progressive, life-long condition that is managed with lifestyle found in the majority of patients changes and medications with HF. HF results from cardiovascular conditions, including chronic hypertension, coronary artery disease, and valvular disease. Ischemia causes myocardial dysfunction because it deprives heart cells of mechanism of HF oxygen and causes cellular 1. impaired contractile properties of the heart (systolic damage. dysfunction) 2. filling of the heart (diastolic) that leads to a lower- than-normal Myocardial infarction (MI) cardiac output. causes focal heart muscle The low cardiac output can lead to compensatory mechanisms necrosis, the death of myocardial that cause increased workload on the heart and eventual cells, and a loss of contractility; resistance to filling of the heart. the extent of the infarction correlates with the severity of HF. Systemic or pulmonary hypertension increases afterload (resistance to ejection), increasing the cardiac workload and leading to the hypertrophy of myocardial muscle fibers. Cardiomyopathy disease of the myocardium. lead to HF and arrhythmias. Dilated cardiomyopathy (DCM) most common type of cardiomyopathy, causes diffuse myocyte necrosis and fibrosis, and commonly leads to progressive HF Valvular heart disease also a cause of HF becomes increasingly difficult for blood to move forward, increasing pressure within the heart and increasing cardiac workload, leading to HF NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Clinical Manifestations Medical Management The signs and symptoms of HF can be Improvement of cardiac function with related to which ventricle is affected. optimal pharmacologic management Left-sided HF (left ventricular failure) causes Reduction of symptoms and improvement of different manifestations than right-sided HF functional status (right ventricular failure). Stabilization of patient condition and In chronic HF, patients may have signs and lowering of the risk of hospitalization symptoms of both left and right ventricular Delay of the progression of HF and extension failure. of life expectancy dyspnea Promotion of a lifestyle conducive to cardiac fatigue --> limit exercise tolerance health fluid retention --> lead to congestion, evidenced by pulmonary and peripheral oral and IV medications edema major lifestyle changes supplemental oxygen Right and Left heart failure have the diff. implantation of assistive devices Manifestation surgical approaches Left-sided heart failure/ left ventricular failure restriction of dietary sodium inability of the left ventricle to fill or eject avoidance of excessive fluid intake, alcohol, sufficient blood into the systemic circulation and smoking weight reduction Right-sided heart failure/ right ventricular failure regular exercise inability of the right ventricle to fill or eject sufficient blood into the pulmonary Pharmacologic Therapy circulation. diuretic Angiotensin system blocker chronic HF/ congestive heart failure Beta blocker may have signs and symptoms of both left- and right-sided heart failure. patient with pulmonary edema acute decompensation, warranting expeditious treatment. Assessment and Diagnostic Methods Assessment of ventricular function Echocardiogram --> ejection fraction (EF) chest x-ray 12 Lead electrocardiogram (ECG) Laboratory studies: serum electrolytes blood urea nitrogen (BUN) creatinine thyroid-stimulating hormone (TSH) CBC count brain natriuretic peptide (BNP) routine urinalysis Cardiac stress testing cardiac catheterization NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Surgical management Left-Sided HF Px w/ CAD Most often precedes right-sided Coronary artery revascularization with PCI cardiac failure Coronary artery bypass surgery Pulmonary congestion Px w/ sever left ventricular dysfunction left ventricle cannot effectively pump placement of ICD blood out of the ventricle into the aorta and the systemic circulation. Px w/ HF who do not improve from standard therapy cardiac resynchronization therapy (CRT) --> Manifestation use biventricular pacemaker dyspnea cough Px w/ severe fluid overload pulmonary crackles ultrafiltration --> use dual lumen central IV low oxygen saturation levels catheter extra heart sound--> S3 or ventricular gallop Right-Sided HF right side cannot eject blood effectively and cannot accommodate all of the blood that normally returns to it from the venous circulation. When the right ventricle fails, congestion in the peripheral tissues and the viscera DOE -- Dyspnea on exertion predominates. When lying flat Increased venous pressure --> jugular venous distention (JVD) manifestations dependent edema (edema of the lower extremities) hepatomegaly (enlargement of the liver) ascites (accumulation of fluid in the peritoneal cavity) weight gain bcos of fluide retentiom. Edema --> feet and ankles Anorexia and nausea Congestive Heart Failure Right-sided heart failure can sometimes occur as a result of left- sided failure. Pulmonary Edema/acute decompensated heart failure acute event, reflecting a breakdown of physiologic compensatory mechanisms occur following acute MI or as an exacerbation of chronic HF. NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - TERMINOLOGIES 14. murmurs: 1. afterload: sounds created by abnormal, turbulent flow of blood in the amount of resistance to ejection of blood from the heart the ventricle 15. myocardial ischemia: 2. apical impulse (also called point of maximum condition in which heart muscle cells receive less oxygen impulse): than needed impulse normally palpated at the fifth intercostal space, left midclavicular line; caused by contraction 16. normal heart sounds: of the left ventricle sounds produced when the valves close; normal heart 3. atrioventricular (AV) node: sounds are S1 (atrioventricular valves) and S2 secondary pacemaker of the heart, located in the (semilunar valves) right atrial wall near the tricuspid valve 17.postural (orthostatic) hypotension: 4. baroreceptors: a significant drop in blood pressure (usually 10 mm Hg nerve fibers located in the aortic arch and carotid systolic or more) after an upright posture is assume arteries that are responsible for reflex control of the blood pressure 18. preload: degree of stretch of the cardiac muscle fibers at the end 5. cardiac catheterization: of diastole an invasive procedure used to measure cardiac chamber pressures and assess patency of the 19. repolarization: coronary arteries return of the cell to resting state, caused by reentry of potassium into the cell while sodium exits the cell 6. cardiac conduction system: specialized heart cells strategically located 20. S1: throughout the heart that are responsible for the first heart sound produced by closure of the methodically generating and coordinating the atrioventricular (mitral and tricuspid) valves transmission of electrical impulses to the myocardial cells 21. S2: the second heart sound produced by closure of the 7. cardiac output: semilunar (aortic and pulmonic) valves amount of blood pumped by each ventricle in liters per minute 22. S3: an abnormal heart sound detected early in diastole as 8. cardiac stress test: resistance is met to blood entering either ventricle; most a test used to evaluate the functioning of the heart often due to volume overload associated with heart during a period of increased oxygen demand failure 9. cardiomyopathy: 23. S4: disease of the heart muscle an abnormal heart sound detected late in diastole as resistance is met to blood entering either ventricle 10. contractility: during atrial contraction; most often caused by ability of the cardiac muscle to shorten in response hypertrophy of the ventricle to an electrical impulse 24. systole: 11. depolarization: period of ventricular contraction resulting in ejection of electrical activation of a cell caused by the influx of blood from the ventricles into the pulmonary artery and sodium into the cell while potassium exits the cell aorta 12. diastole: 25. telemetry: period of ventricular relaxation resulting in the process of continuous electrocardiographic ventricular filling monitoring by the transmission of radio waves from a battery-operated transmitter worn by the patient 13. hemodynamic monitoring: use of pressure monitoring devices to directly measure cardiovascular function  ⬇ ⬆ ⬇ NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - WK2:CU2-- CORONARY ARTERY DISEASES ANGINA PECTORIS AND MYOCARDIAL INFARCTION 1. Coronary Atherosclerosis and CAD 1. Coronary Atherosclerosis 2. Angina Pectoris most common cause of cardiovascular disease in the United States 3. Myocardial Infarction abnormal accumulation of lipid or fatty substances and fibrous tissue in the vessel wall --> block or narrow the vessel, reducing blood flow to the myocardium. Connection ng tatlo: Pathophysiology Cholesterol-containing deposits begins with injury to the vascular endothelium and progresses over (plaques) lodge in your coronary arteries many years injury may be initiated by smoking or tobacco use, hypertension, buildup of plaque can narrow these hyperlipidemia, and other factors. arteries, decreasing blood flow to your The endothelium undergoes changes and stops producing the heart. normal antithrombotic and vasodilating agents. (coronary atherosclerosis) The presence of inflammation attracts inflammatory cells, such as macrophages. reduced blood flow may cause The macrophages ingest lipids, becoming “foam cells” that transport chest pain (angina pectoris) the lipids into the arterial wall. shortness of breath Some of the lipid is deposited on the arterial wall, forming fatty other CAD s and sx streaks. Activated macrophages also release biochemical substances that can further damage the endothelium by contributing to the oxidation of complete blockage can cause a heart low-density lipoprotein (LDL). attack. The oxidized LDL is toxic to the endothelial cells and fuels (Myocardial infarction) progression of thenatherosclerotic process Following the transport of lipid into the arterial wall, smooth muscle Coronary artery disease (CAD) cells proliferate and form a fibrous cap over a core filled with lipid develops when the major blood and inflammatory infiltrate. vessels that supply your heart become These deposits, called atheromas, or plaques, protrude into the damaged or diseased. lumen of the vessel, narrowing it and obstructing blood flow. Plaque may be stable or unstable, depending on the degree of inflammation and thickness of the fibrous cap. If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can resist the stress of blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable plaque. At this point, the lipid core may grow, causing the fibrous plaque to rupture. A ruptured plaque attracts platelets and causes thrombus formation. A thrombus may then obstruct blood flow, leading to acute coronary syndrome (ACS), which may result in an acute myocardial infarction (MI). When an MI occurs, a portion of the heart muscle no longer receives blood flow and becomes necrotic. Risk Factors roma athe Modifiable High blood cholesterol (hyperlipidemia) LDL - bad cholesterol Non Modifiable I HDL - good cholesterol Positive family triglycerides history hypertension Age ( 45y.o = men, Hyperlipidemia 55y.o = women) Hyperglycemia (diabetes mellitus) Gender Obesity (men>women) Race (African lodge to Physical inactivity Cigarette smoking, tobacco use Americans) Metabolic syndrome History of premature circulation pulmonary" embolism Enlarged waist circumference chronic inflammatory conditions menopause Primary Chronic kidney disease hypercholesterolemia  ⬆ ⬇ NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza Symptoms include the following: Ischemia --> blood supply Chest pain: angina pectoris Atypical symptoms of myocardial ischemia (shortness of breath, nausea, and weakness) Myocardial infarction Dysrhythmias, sudden death Assessment and Diagnostic Methods thorough history, including family history physical examination (note blood pressure and weight) laboratory work (eg, cholesterol levels [low-density lipoprotein (LDL) to high-density lipoprotein (HDL)], glucose). Prevention Four modifiable risk factors 1. cholesterol abnormalities 2. tobacco use 3. hypertension 4. diabetes mellitus AHA Guidelines that addresses this prevention 1. cholesterol levels LDL = ACS Pathophysiology exercise or pharmacologic stress test Angina is usually caused by atherosclerotic disease nuclear scan or invasive procedure (e.g., cardiac myocardium extracts a large amount of oxygen from the catheterization, coronary angiography). coronary circulation to meet its continuous demands. When demand increases, flow through the coronary Medical Management arteries needs to be increased. decrease the oxygen demand of the myocardium When there is a blockage in a coronary artery, flow and to increase the oxygen supply. cannot be increased and ischemia results. reperfusion procedures Several factors associated w/ anginal pain: --> restore the blood supply to the myocardium. 1. Physical exertion --> mycardial oxygen demand 2. Exposure to cold --> vasoconstriction, BP, oxygen 1. PCI procedures (eg, percutaneous transluminal demand coronary angioplasty [PTCA], intracoronary stents, and atherectomy) 3. Eating heavy meal --> blood flow to mesenteric area 2. coronary artery bypass graft (CABG). for digestion --> blood supply available to heart muscle Pharmacologic Therapy 4. Stress --> release catecholamines --> BP, HR, myocardial workload 1. Nitroglycerin/Nitrates standard treatment Types of Angina Potent vasodilator Improve blood flow to the heart muscle 1. Stable angina Relieves pain predictable and consistent pain Adverse effect: HEADACHE occurs on exertion relieved by rest and/or nitroglycerin 2. Beta-adrenergic blockers -olol meds 2. Unstable angina reduce myocardial oxygen consumption by preinfarction angina/crescendo angina blocking beta adrenergic sympathetic stimulation symptoms increase in frequency and severity to heart may not be relieved with rest or nitroglycerin in heart rate Slowed conduction of impulses 3. Intractable or refractory angina BP severe incapacitating chest pain myocardial contractility 4. Variant angina/Prinzmetal’s angina MONITOR BP pain at rest with reversible ST-segment elevation caused by coronary artery vasospasm 3. Calcium channel blockers/calcium ion antagonists amlodipine and diltiaze 5. Silent ischemia SA node automaticity, AV node conduction objective evidence of ischemia Slower HR patient reports no pain strength of myocardial contraction workload of heart Clinical Manifestations mild indigestion to a choking or heavy sensation in the upper chest The patient with diabetes mellitus may not experience 4. Antiplatelet and anticoagulant medications severe pain with angina --> block pain, sensation aspirin --> prevent platelet aggregation accompanied by severe apprehension and a feeling of clopidogrel --> addition to aspirin for px risk for impending death. MI pain in retrosternal, deep in the chest behind the upper heparin --> prevent formation of new blood clots or middle third of the sternum. glycoprotein --> for px w/ unstable angina; PCI pain radiate to the neck, jaw, shoulders, and inner aspect of the upper arms (usually the left arm). feeling of weakness or numbness in the arms, wrists, 6. Oxygen therapy and hands initiated at onset of chest pain Increase oxygen delivered to mycardium --> shortness of breath pallor pain diaphoresis dizziness nausea and vomiting Anxiety NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Nursing Interventions III. Acute Coronary Syndrome and Myocardial Infarction Treating Angina Direct the patient to stop all activities and sit acute onset of myocardial ischemia that results in or rest in bed in a semi-Fowler’s position to myocardial death reduce the oxygen requirements of the ischemic myocardium. Pathophysiology Measure vital signs and observe for signs of reduced blood flow in a coronary artery respiratory distress. due to rupture of an atherosclerotic plaque Administer nitroglycerin Clot begins to form on top of the coronary lesion but the Administer oxygen therapy artery is not completely occluded. This is a preinfarction angina because the patient will likely Reducing Anxiety have an MI if prompt interventions do not occur. Provide essential information about the In an MI, plaque rupture and subsequent thrombus illness and methods of preventing formation result in complete occlusion of the artery progression. leading to ischemia and necrosis of the myocardium Explore various stress reduction methods supplied by that artery. with patient (eg, music therapy). other causes of MI Preventing Pain Vasospasm identify the level of activity that causes the sudden constriction or narrowing of a coronary artery patient’s pain or prodromal symptoms, Balancing activity and rest is an important decreased oxygen supply aspect of the educational plan for the patient from acute blood loss, anemia, or low blood pressure and family. increased demand for oxygen from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine) The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction, or the death of cells. The expression “time is muscle” reflects the urgency of appropriate treatment to improve patient outcomes. Clinical Manifestations Chest pain that occurs suddenly and continues despite rest and medication. prodromal symptoms or a previous diagnosis of coronary artery disease (CAD) chest pain, shortness of breath, indigestion, nausea, and anxiety. cool, pale, and moist skin heart rate and respiratory rate may be faster than normal. Assessment and Diagnostic Methods Patient history description of presenting symptom history of previous illnesses family health history, particularly of heart disease) 12 lead Electrocardiography (ECG) obtained within 10 minutes of pain T wave inversion, ST segment , abnormal Q wave Echocardiogram evaluate ventricular function Detect hypokinetic and akinetoc wall motion Lab test Cardiac enzymes and biomarkers (creatine kinase isoenzymes, myoglobin, and troponin).  ⬇ NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - Medical Management 4. Inpatient Management to minimize myocardial damage preserve myocardial function cardiac intensive care unit (ICU) prevent complications Following PCI or thrombolytic therapy, continuous cardiac increasing oxygen supply with monitoring is indicated medications oxygen administration Continuing pharmacologic management bed rest aspirin beta-blocker 1. Initial Management ACE) inhibitor. supplemental oxygen --> prevent the conversion of angiotensin 1 to angiotensin II. aspirin --> blood pressure nitroglycerin --> kidneys excrete sodium and fluid (diuresis) --> standard treatment --> the oxygen demand of the heart. --> Potent vasodilator --> Improve blood flow to the heart muscle angiotensin receptor blocker (ARB) --> Relieves pain --> If an ACE inhibitor is not suitable --> Adverse effect: HEADACHE Nicotine replacement therapy and tobacco cessation counseling morphine should also be initiated for all --> drug of choice to reduce pain and anxiety tobacco users. --> if nitrates not effective --> reduces preload and afterload 5. Cardiac Rehabilitation --> decreasing the work of the heart After the patient with an MI is in a stable condition, --> monitor for BP, RR providing patient and family education, offering individual and group support, and encouraging physical activity and physical beta blocker conditioning. --> not need for initial mngmt --> introduced w/in 24 hr of admission Goals --> for arrhythmias to extend life and improve the qualiy of life. Objectives heparin to limit the effects and progression of atherosclerosis --> prevent further clot formation return the patient to work and a pre-illness lifestyle enhance the patient’s psychosocial and vocational status 2. Emergent Percutaneous Coronary prevent another cardiac event. Intervention (PCI) in cardiac catheterization laboratory three phases to open the occluded coronary artery and promote reperfusion to the area that has Phase I been deprived of oxygen. begins with the diagnosis of atherosclerosis, which may occur initial treatment method for acute MI in when the patient is admitted to the hospital for ACS. all age groups focuses on the essentials of self-care rather than instituting behavioral changes for risk reduction. door-to-balloon time signs and symptoms that indicate the need to call 911 (seek the time from the patient’s arrival in the emergency assistance) ED to the time PCI is performed should be the medication regimen, rest–activity balance, and follow-up less than 60 minutes. appointments with the primary provider. 3. Thrombolytic therapy Phase II when primary PCI is not available after the patient has been discharged. administered IV according to a specific The patient attends sessions three times a week for 4 to 6 weeks protocol but may continue for as long as 6 months. alteplase, reteplase, and tenecteplase. The outpatient program consists of supervised, often ECG- to dissolve the thrombus in a coronary monitored, exercise training that is individualized. artery (thrombolysis), allowing blood to assessed for the effectiveness of and adherence to the treatment. flow through the coronary artery again educational sessions for patients and families that are given by (reperfusion), minimizing the size of the cardiologists, exercise physiologists, dietitians, nurses, and other infarction and preserving ventricular health care professionals. function. should not be used if the patient is Phase III bleeding or has a bleeding disorder. long-term outpatient program focuses on maintaining cardiovascular stability and long-term door-to-needle time conditioning. should be given within 30 minutes of self-directed during this phase and does not require a supervised symptom onset for best results program NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - INVASIVE CORONARY ARTERY PROCEDURES PERCUTANEOUS CORONARY INTERVENTION Surgical Procedures: Coronary Artery through skin puncture rather than surgical Revascularization incision 1. Coronary Artery Bypass Graft (CABG) 1. Percutaneous Transluminal Coronary surgical procedure Angioplasty (PTCA) Blood vessel is grafted to an occluded coronary artery balloon tipped catheter --> open blocked so that blood can flow beyond the occlusion coronary vessels --> resolved ischemia Also called bypass graft for angina and ACS Purpose: improved blood flow within Indications coronary artery by compressing atheroma alleviation of angina, not controlled with medication or PCI 2. Coronary Artery Stent treatment for left main coronary artery stenosis or stent is a metal mesh that provides multivessel CAD structural support to a vessel at risk of prevention of and treatment for MI, dysrhythmias or acute closure heart failure there are risk for thrombus formation Treatment for complications from an unsuccessful within the stent --> antiplatelet PCI medications (aspirin and clopidogrel) Aspirin should be continued indefinitely internal mammary artery used for CABG and clopidogrel is continued for 1 year arterial grafts are preferred to venous grafts because following stent placement they do not develop atherosclerotic 3. Post procedure care A vein commonly used for CABG is the greater during the PCI, patients received IV saphenous vein, followed by the lesser saphenous vein heparin or a thrombin inhibitor and are Endovascular methods of vein harvesting have monitored closely for signs of bleeding reduced complications such as infection and wound GP llb/lla agent --> prevent platelet dehiscence. aggregation and thrombus formation in 2. Traditional Coronary Artery Bypass Graft the coronary artery performed under general anesthesia. Hemostasis is achieved, and femoral surgeon performs a median sternotomy and connects sheaths may be removed at the end of the the patient to the cardiopulmonary bypass (CPB) procedure by using a vascular closure machine. device Next, a blood vessel from another part of the patient’s Hemostasis after sheat removal may also body (eg, saphenous vein, left internal mammary be achieved by direct manual pressure, a artery) is grafted distal to the coronary artery lesion, mechanical compression device. bypassing the obstruction CPB is then discontinued, chest tubes and epicardial pacing wires are placed, a critical care unit. Cardiopulmonary Bypass Many cardiac surgical procedures are possible because of CPB thos procedure mechanically circulates and oxygenates blood for the body while bypassing the heart and lungs. CPB maintains perfusion to body organs and tissues and allows the surgeon to complete the anastomoses in a motionless, bloodless surgical field. Off-pump coronary artery bypass (OPCAB) alternative CABG techniques involves a standard median sternotomy incision, but the surgery is performed without CPB. beta-adrenergic blocker --> slow the heart rate. uses a myocardial stabilization device to hold the site still for the anastomosis of the bypass graft into the coronary artery while the heart continues to beat NCMB312: Medical Surgical Third Year: First Semester - Prelim Professor: Annabelle Flores Transcriber: Nicole Kristin Canoza - TERMINOLOGIES 1. acute coronary syndrome (ACS): signs and symptoms that indicate unstable angina or acute myocardial infarction 2. angina pectoris: chest pain brought about by myocardial ischemia 3. atheroma: fibrous cap composed of smooth muscle cells that forms over lipid deposits within arterial vessels and protrudes into the lumen of the vessel, narrowing the lumen and obstructing blood flow; also called plaque 4. atherosclerosis: abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and the lumen 5. contractility: ability of the cardiac muscle to shorten in response to an electrical impulse 6. coronary artery bypass graft (CABG): a surgical procedure in which a blood vessel from another part of the body is grafted onto the occluded coronary artery below the occlusion in such a way that blood flow bypasses the blockage 7. creatine kinase (CK): an enzyme found in human tissues; one of the three types of CK is specific to heart muscle and may be used as an indicator of heart muscle injury 8. high-density lipoprotein (HDL): protein-bound lipid that transports cholesterol to the liver for excretion in the bile; composed of a higher proportion of protein to lipid than low-density lipoprotein; exerts a beneficial effect on the arterial wall 9. ischemia: insufficient tissue oxygenation 10. low-density lipoprotein (LDL): a protein-bound lipid that transports cholesterol to tissues in the body; composed of a lower proportion of protein to lipid than high-density lipoprotein; exerts a harmful effect on the arterial wall 11. metabolic syndrome: a cluster of metabolic abnormalities including insulin resistance, obesity, dyslipidemia, and hypertension that increase the risk of cardiovascular disease 12. myocardial infarction (MI): death of heart tissue caused by lack of oxygenated blood flow 13. percutaneous coronary intervention (PCI): an invasive procedure in which a catheter is placed in a coronary artery, and one of several methods is employed to remove or reduce a blockage within the artery 14. percutaneous transluminal coronary angioplasty (PTCA): a type of percutaneous coronary intervention in which a balloon is inflated within a coronary artery to break an atheroma and open the vessel lumen, improving coronary artery blood flow 16. stent: a woven mesh that provides structural support to a coronary vessel, preventing its closure 17. sudden cardiac death: abrupt cessation of effective heart activity 18. thrombolytic: an agent or process that breaks down blood clots 19. troponin: myocardial protein; measurement is used to assess heart muscle injury