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NUR435 Adult- Exam 2
NUR 435 Adult- Exam 2
| Question | Answer |
|---|---|
| Infection of the inner layer (endocardial) of the heart that usually affects the cardiac valves. | infective endocarditis |
| clinical manifestations include: Arthralgias Myalgias Back pain Abdominal discomfort Weight loss Headache Clubbing of fingers | subacute form infective endocarditis |
| vascular manifestations include: Splinter hemorrhages in nail beds Petechiae Osler’s nodes on fingers or toes Janeway’s lesions on palms or soles Roth’s spots | subacute form infective endocarditis |
| clinical manifestations include: Murmur in most patients (new onset) Heart failure in up to 80% with aortic valve endocarditis Manifestations secondary to embolism | subacute form infective endocarditis |
| characterized by: Longer clinical course Insidious onset Caused by enterococci Affects those with preexisting valve disease | subacute form infective endocarditis |
| characterized by: shorter clinical course rapid onset usually affects those with healthy valves | acute form infective endocarditis |
| causative organisms include: Streptococcus viridans Staphylococcus aureus Viruses Fungi | infective endocarditis |
| principal risk factors for infective endocarditis | Prior endocarditis Prosthetic valves Acquired valvular disease Cardiac lesions |
| vegetation | Fibrin, leukocytes, platelets, and microbes Adhere to the valve or endocardium Embolization of portions of vegetation into circulation |
| main contributing risk factors include: Aging, IVDA, prosthetic valve, renal dialysis, nosocomial infections resulting from intravascular device placement | infective endocarditis |
| signs and symptoms: Fever, chills, weakness, malaise, fatigue, and anorexia | infective endocarditis |
| history taken should include: Recent dental, urologic, surgical, or gynecological procedures Heart disease Recent cardiac catheterization Skin, respiratory, or urinary tract infection | infective endocarditis |
| laboratory diagnostics for infective endocarditis | Blood cultures (two drawn 30 minutes apart; positive in most) WBC with differential |
| diagnostic tests for infective endocarditis | ECG and chest x-ray |
| major criteria to diagnose infective endocarditis | Patient must have two of the following: Positive blood cultures New or changed cardiac murmur Intracardiac mass or vegetation noted on echocardiography |
| collaborative care for infective endocarditis includes | prophylactic treatment for some and antibiotic administration |
| prophylactic treatment for infective endocarditis for patients having | Removal or drainage of infected tissue Renal dialysis Ventriculoatrial shunts used for hypdrocephalus |
| antibiotic administration for infective endocarditis should include | Monitor antibiotic serum levels Subsequent blood cultures Renal function monitored |
| infective endocarditis that responds poorly to antibiotics | Fungal and prosthetic valve endocarditis |
| infective endocarditis that responds poorly to antibiotics should have this as an adjunct procedure | valve replacement |
| subjective data of nursing assessment should include: includes history of valvular, congenital, or syphilitic cardiac disease; previous endocarditis; staph or strep infection; immunosuppressive therapy; and recent surgeries and procedures | infective endocarditis |
| functional health patterns to be documented should include: IV drug abuse, alcohol abuse, weight changes, and chills. | infective endocarditis |
| other s/s to include in nursing assessment: diaphoresis, bloody urine, exercise intolerance, generalized weakness, fatigue, cough, dyspnea on exertion, night sweats, chest, back, or abdominal pain | infective endocarditis |
| objective data should also include: Tachypnea Crackles Dysrhythmias New/changed murmur Tachycardia Leukocytosis Anemia Increased ESR* and cardiac enzymes Positive cultures ECG showing chamber enlargement | infective endocarditis |
| (painful, tender, red or purple, pea-size lesions) may be found on the fingertips or toes. | Osler's nodes |
| flat, painless, small, red spots) may be found on the palms and soles. | Janeway's lesions |
| implementation and teaching: Adherence to treatment regimen. Avoid infectious people. Avoid stress and fatigue. Rest, hygiene, and nutrition. Monitor labs, IV patency. ROM TCDB s/s of infection; reduction measures for risk for infection. Follow-up care. | infective endocarditis |
| evaluation should include: vital signs; absence of chills, diaphoresis, headache; sufficient cardiac output; completion of ADLs with no fatigue or physiologic distress; and increased understanding of disease process and self-care management | infective endocarditis |
| most often idiopathic with a variety of suspected viral causes. Caused by inflammation of the pericardial sac (pericardium) | acute pericarditis |
| other causes may include: Uremia Bacterial infection Acute myocardial infarction (MI) Tuberculosis Neoplasm Trauma | acute pericarditis |
| hallmark finding is pericardial friction rub | acute pericarditis and Dressler syndrome |
| Clinical manifestations include progressive, frequent severe chest pain…..worse with deep inspiration and when lying supine. | acute pericarditis |
| associated with pericardial effusion and cardiac tamponade | acute pericarditis |
| Accumulation of excess fluid in the pericardium Compression results in: cough, dyspnea, tachypnea Nerve compression can induce hiccups and/or hoarseness BP is maintained by compensatory mechanisms | pericardial effusion |
| Develops as the pericardial effusion increases in volume resulting in compression of the heart Can occur acutely (rupture of heart, trauma) or subacutely (secondary to malignancy, uremia) Pt may become confused, anxious, and restless | cardiac tamponade |
| diagnostic studies should include: EKG Chest x-ray to check for cardiomegaly Echocardiogram Magnetic resonance imaging (MRI) Computed tomography (CT) | acute pericarditis |
| lab findings include: Leukocytosis Elevated C-reactive Protein (CRP) and ESR | acute pericarditis |
| Collaborative Care includes identifying and treating the underlying problem, bed rest, medications (ASA, NSAIDS, and corticosteroids). These patients may need to have a pericardiocentesis | acute pericarditis |
| Performed for pericardial effusion with acute cardiac tamponade Complications may include: dysrhythmias, pneumothorax, coronary artery laceration, myocardial laceration, etc. | pericardiocentesis |
| The primary nursing consideration is the patient’s pain and anxiety. | acute pericarditis |
| pain: Usually located in the left trapezius ridge Sharp, pleuritic quality that increases with inspiration Often relieved by sitting or leaning forward; worsens when lying supine | acute pericarditis |
| pain relief measures for acute pericarditis | Elevate head of bed to 45 degrees Provide an overbed table for support Give antiinflammatory medications as ordered along with teaching |
| anxiety reducing measures for acute pericarditis | Provide simple, complete explanations of all procedures performed and possible cause of pain |
| Monitor for signs and symptoms of tamponade Make preparations for possible pericardiocentesis | acute pericarditis |
| it can involve all layers of the heart and other areas as well such as joints, CNS, and skin | rheumatic heart disease |
| it occurs as a delayed sequela of group A streptococcal pharyngitis | rheumatic heart disease |
| must be evidence of preceding group A streptococcal infection | rheumatic heart disease |
| most important manifestation of rheumatic heart disease | carditis: Organic heart murmur, mitral/aortic regurgitation, or mitral stenosis Cardiac enlargement and heart failure secondary to myocarditis Percarditis |
| most common finding of rheumatic heart disease | Mono- or polyarthritis |
| major CNS manifestation of rheumatic heart disease | chorea |
| major criteria may include: Erythema marginatum lesions Subcutaneous nodules | rheumatic heart disease |
| associated with: Fever Polyarthralgia Increased ESR, WBC count, CRP | rheumatic heart disease |
| most often involved with chronic rheumatic carditis | mitral valve |
| supportive measures for acute rheumatic fever | Drug therapy Antibiotics Corticosteroids Salicylates Nonsteroidal antiinflammatory drugs (NSAIDS) Supportive measures Bed rest |
| subjective data: Past health history Recent streptococcal infection Previous history of rheumatic fever or rheumatic heart disease | rheumatic heart disease |
| functional health patterns: Family history Malaise Anorexia, weight loss Generalized weakness or fatigue Palpitations Chest pain Migratory joint pain and tenderness | rheumatic heart disease |
| objective data: Fever Subcutaneous nodules Rashes Involuntary, purposeless, rapid motions Facial grimaces Swelling, heat of joints Tachycardia Pericardial friction rub Murmurs Peripheral edema Cardiomegaly on chest x-ray | rheumatic heart disease |
| teach the patient to seek medical attention for symptoms of strep pharyngitis and need for treatment of this infection | rheumatic heart disease health promotion |
| interventions include control and eradicate infection; prevent cardiac complications; relieve joint pain, fever, symptoms; promote rest; have pt ambulate after acute symptoms have subsided; and encourage nonstrenous activities once recovery has begun | rheumatic heart disease |
| Evaluate ability to perform ADLs with little fatigue and pain; adherence to treatment regimen, and confidence in managing the disease | rheumatic heart disease |
| type depends on valve or valves affected | valvular heart disease |
| 2 types of functional alterations with valvular heart disease | stenosis and regurgitation |
| Valve orifice is restricted | stenosis |
| Impeding forward blood flow | stenosis |
| Creates a pressure gradient across open valve Degree reflected in pressure gradient differences | stenosis |
| Incomplete closure of valve leaflets | regurgitation |
| Results in backward flow of blood | regurgitation |
| occur in children and adolescents primarily from congenital conditions | valvular disorders |
| occur in adults from degenerative heart disease | valvular disorders |
| majority of adult cases of valvular heart disease result from | rheumatic heart disease |
| Scarring valve leaflets & chordae tendineae. Contractures, adhesions between commissures of leaflets. Stenotic MV “fish mouth” shape from thickening shortening. Obstruction. Increase LA pressure, volume. Hypertrophy pulmo vessels. LA pressure elevations. | why rheumatic heart disease causes valvular heart disease |
| most common cause of valvular heart disease | rheumatic heart disease |
| clinical manifestations: Dyspnea Palpitations from atrial fibrillation. Fatigue. Accentuated first heart sound. Low-pitched, rumbling diastolic murmur. Hoarseness. Chest pain. Seizures. Stroke. | mitral valve stenosis |
| primary symptom is dyspnea because of reduced lung compliance and occasionally accompanied by hemoptysis | mitral valve stenosis |
| Asymptomatic for years until development of some degree of left ventricular failure | mitral valve regurgitation |
| acute clinical manifestations: Thready peripheral pulses and cool, clammy extremities | mitral valve regurgitation |
| Initial symptoms include: Weakness, fatigue, palpitations, dyspnea that gradually progresses to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema. | mitral valve regurgitation |
| Brisk carotid pulses. Auscultatory findings of accentuated left ventricular filling leading to audible S3. Murmur is loud pansystolic or holosystolic at apex radiating to left axilla. | mitral valve regurgitation |
| Structural abnormality of mitral valve leaflets and papillary muscles or chordae that allow leaflets to prolapse into left atrium during systole. | mitral valve prolapse |
| causes of mitral valve regurgitation | MI Chronic rheumatic heart disease Mitral valve prolapse Ischemic papillary muscle dysfunction Infective endocarditis |
| valvular disorder of unknown etiology | mitral valve prolapse |
| Most asymptomatic for life. Murmur from insufficiency, more intense through systole. Late or holosystolic murmur Clicks mid to late systole, constant or vary beat to beat. Dysrhythmias. Paroxysmal SV tach. V tach: Palpitations, lightheadedness, dizziness | mitral valve prolapse |
| may or may not be present with chest pain | mitral valve prolapse |
| that if a patient presents with aortic valve stenosis with clinical manifestations that include angina, syncope, and exertional dyspnea this reflects | left ventricular failure |
| Nitroglycerin is contraindicated because it reduces preload | valvular heart disease |
| May result from disease of aortic valve leaflets, aortic root, or both | aortic valve regurgitation |
| Caused by: Infective endocarditis Trauma Aortic dissection | aortic valve regurgitation |
| Chronic aortic regurgitation results from | Rheumatic heart disease Congenital bicuspid aortic valve Syphilis Chronic rheumatic heart conditions |
| Sudden manifestations of cardiovascular collapse Left ventricle exposed to aortic pressure during diastole Weakness Severe dyspnea Chest pain Hypotension Constitutes a medical emergency | aortic valve regurgitation |
| you will hear a systolic ejection click | aortic valve regurgitation |
| occurs almost exclusively in patients who are IV drug abusers | tricuspid valve stenosis |
| will see peripheral edema, ascites, hepatomegaly, etc.; it is usually the result of pulmonary hypertension or right ventricular dysfunction | tricuspid valve stenosis |
| almost always congenital and causes right ventricular hypertension and hypertrophy | pulmonic valve stenosis |
| will have fatigue and a loud midsystolic murmur | pulmonic valve disease |
| Treatment depends on the valve involved and severity of the disease | valvular heart disease |
| priority is prevention of recurrent rheumatic fever and infective endocarditis | valvular heart disease |
| Drug therapy includes digitalis, diuretics, antidysrhythmics, beta blockers, and anticoagulants | valvular heart disease |
| therapy includes low sodium diet | valvular heart disease |
| May need a percutaneous transluminal ballon valvuloplasty to open fused commissures | valvular heart disease |
| May need surgical treatment for valve repair or replacement | valvular heart disease |
| Objective data may include tachycardia, abnormal heart sounds, ascites, crackles, wheezes, or hoarseness, diaphoresis, peripheral edema, dysrhythmias, etc | valvular heart disease |
| Implementation includes diagnosing and treating streptococcal infections and providing prophylaxis for history; no smoking; avoid strenuous activity; medical alert bracelet; complete antibiotic regimen; INR for anticoagulation therapy, follow-up care. | valvular heart disease |
| Evaluate for tolerance to increased activity, BP, HR, and breath sounds, no peripheral edema or fatigue, adherence to therapeutic regimen, and knowledge of s/s of when to seek health care and use prophylactic antibiotics | valvular heart disease |
| flow of blood through the heart | IVC & SVC to right atrium to tricuspid valve to right ventricle to pulmonic valve to pulmonary artery to pulmonary veins to left atrium to mitral valve to left ventricle to aortic valve to aorta to circulation |
| not a disease but a syndrome | heart failure |
| an abnormal condition involving impaired cardiac pumping resulting in physiologic changes in vasoconstriction and fluid retention | heart failure |
| associated with hypertension, CAD, and MI | heart failure |
| CAD, hypertension, anemia, and cardiomyopathy are causes | chronic heart failure |
| causes include acute MI, dysrhythmias, pulmonary emboli | acute heart failure |
| two primary risk factors for heart failure | CAD and advancing age |
| contributing risk factors: Hypertension Diabetes Tobacco use Obesity High serum cholesterol African American descent | heart failure |
| most common cause of heart failure | Systolic failure; the heart is unable to pump blood appropriately |
| Hallmark finding: Decrease in the left ventricular ejection fraction (EF). EF: fraction of blood pumped out of a ventricle with each heart beat | systolic heart failure |
| Caused by: Impaired contractile function Increased afterload (Afterload can be thought of as the “force" that the heart must eject blood against) Cardiomyopathy (disease of the heart muscle) Mechanical abnormalities | systolic heart failure |
| Results from impaired ability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and cardiac output | diastolic failure |
| Diagnosis Based on the presence of …. pulmonary congestion pulmonary hypertension ventricular hypertrophy normal ejection fraction | diastolic heart failure |
| caused by: Left ventricular hypertrophy from chronic hypertension Aortic stenosis Hypertrophic cardiomyopathy Isolated right ventricular diastolic failure from pulmonary hypertension. | diastolic heart failure |
| Seen more frequently in older adult women | diastolic heart failure |
| most common heart failure | left sided heart failure |
| left sided heart failure is most commonly result of | left ventricular dysfunction |
| causes of left ventricular dysfunction include | MI, HTN, CAD, cardiomyopathy |
| What would you expect to see if a patient has left sided heart failure? | Blood backs up into the left atrium and pulmonary veins Pulmonary congestion Pulmonary edema |
| What would you expect to see if a patient has right sided heart failure? | Blood backs up into the right atrium and venous systemic circulation. Jugular venous distention (JVD) Hepatomegaly, splenomegaly Ascites Peripheral edema |
| causes of right sided heart failure | Left sided heart failure Cor pulmonale (change in structure and function of the right ventricle of the heart as a result of a respiratory disorder) Right ventricular MI |
| What would you expect to see in your patient in the early stages of acute heart failure? | Increase in the respiratory rate Decrease in PaO2 |
| What would you expect to see in your patient in the later stages of acute heart failure? | Tachypnea Respiratory acidosis |
| What do you see that is often life threatening to the patient with acute heart failure? | Acute decompensated heart failure (ADHF) Pulmonary edema, often life-threatening |
| physical findings of acute heart failure | Orthopnea Dyspnea, tachypnea Use of accessory muscles Cyanosis Cool and clammy skin Cough with frothy, blood-tinged sputum Breath sounds: crackles or rales, wheezes, rhonci Tachycardia Hypotension or hypertension |
| clinical manifestations: fatigue, dyspnea, dependent edema, anorexia, nausea, restlessness, confusion, decreased memory, skin, nocturia | chronic heart failure |
| Edema that changes its position with the posture of dependent parts (for example, edema of the legs in progressive heart failure) | dependent edema |
| compensation in heart failure results from | SNS activation, neurohormonal response, dilation, and hypertrophy |
| Release of catecholamines; Will see increased HR; increased myocardial contractility; peripheral vasoconstriction | SNS activation as compensation for heart failure |
| Kidneys release renin: RAAS is activated Sodium & water retention Increase BP perfusion pressure Antidiuretic hormone released resulting in water retention and increase in blood volume | neurohormonal response as compensation for heart failure |
| Endothelin stimulated by ADH, catecholamines, & angiotension II Hypertrophy, arterial vasoconstriction, inc cardiac contractility Proinflammatory cytokines are released Myocytes released due to cardiac injury; depress cardiac function | neurohormonal response as compensation for heart failure |
| Enlargement of the chambers of the heart resulting from elevated pressure in LV Initially an adaptive mechanism; eventually becomes inadequate & CO decreases | dilation as compensation for heart failure |
| Increase in muscle mass & cardiac wall thickness in response to dilation Heart muscle has poor contractility; higher O2 needs, poor coronary artery circulation, & prone to ventricular Dysrhythmias | hypertrophy as compensation for heart failure |
| mechanisms succeed in maintaining adequate CO for tissue perfusion | compensation in heart failure |
| mechanisms no longer maintain adequate CO thus inadequate tissue perfusion | decompensation in heart failure |
| Results of activation of SNS and NH response Hypertrophy of cardiac myocytes, results in large abnormal cells Can't contract as well Increased ventricular muscle mass, change ventricular shape and dimension Impaired contractility is the consequence | ventricular remodeling |
| what is BNP (b-type natriuretic peptide)? | Promote venous and arterial vasodilation, reducing preload and afterload, Enhance diuresis, Block effects of RAAS, 32-AA peptide secreted primarily from the ventricles of heart in response to stretch and increased volume in ventricles |
| BNP levels correlate with and why it is important to measure in HF patients? | left ventricular pressure/volume and NYHA classification Rapid, point of care assay for BNP now available to facilitate diagnosis of HF and use as a prognostic marker |
| primary goal of diagnostic studies for heart failure | determine underlying cause |
| diagnostic studies include: History and physical examination Chest x-ray ECG Lab studies for Elevated BNP level* Echocardiogram* to determine Ejection Fraction | heart failure |
| Overall goals of therapy for ADHF and chronic HF: | Decrease patient symptoms Improve LV function Reverse ventricular remodeling Improve quality of life Decrease mortality and morbidity |
| to decrease intravascular volume (reduces venous return and preload) in heart failure | loop diuretics (furosemide) and ultrafiltration |
| to decrease venous return (preload) (reduces the amt of volume returned to LV during diastole) in heart failure | High-Fowler’s position IV Nitroglycerin |
| to decrease afterload (improves CO and decreases pulmonary congestion) in heart failure | Morphine sulfate Dilates systemic blood vessels Dilates pulmonary blood vessels Reduces anxiety IV sodium nitroprusside (Nipride) Nesiritide (Natrecor) – recombinant form of BNP |
| to improve gas exchange and oxygenation in heart failure | Supplemental oxygen Morphine sulfate Noninvasive ventilator support such as BiPAP Intubation and mechanical ventilation |
| to improve cardiac function in patients that do not respond to conventional pharmacotherapy | implement inotropic therapy (beta-adrenergic agonists and phosphodiesterase inhibitors), hemodynamic monitoring, and reduce anxiety |
| Increase in contractility IV infusion, short term Examples: Dopamine- increases BP, dilates renal blood vessels Dobutamine- works selectively on receptors in heart, no increase in BP | beta-adrenergic agonists to improve cardiac function in patients that do not respond to conventional pharmacotherapy |
| Increase myocardial contractility Promote vasodilation Increase cardiac output while reducing arterial pressure Examples Inamrinone (Inocor) Milrinone (Primacor) | phosphodiesterase inhibitors to improve cardiac function in patients that do not respond to conventional pharmacotherapy |
| methods of reducing anxiety to improve cardiac function in patients that do not respond to conventional pharmacotherapy | Distraction, imagery Sedative medications (e.g., morphine sulfate, benzodiazepines) |
| Main treatment goal for is treat the underlying cause and contributing factors | chronic heart failure |
| may be treated with diuretics, vasodilators, and positive inotropic agents such as digitalis | chronic heart failure |
| diuretics used to treat chronic heart failure | Thiazide Loop Spironolactone |
| vasodilators used to treat chronic heart failure | ACE inhibitors Angiotensin II receptor blockers Nitrates beta-Adrenergic blockers |
| positive inotropic agents used to treat chronic heart failure | digitalis and calcium sensitizers |
| Increases force of contraction Slows heart rate Watch for signs of toxicity: anorexia, N/V, visual disturbances, dysrhythmias. Enhanced in hypokalemia. | digitalis |
| Improve contractility without increasing myocardial work (e.g. levosimendan) In clinical trials at present | calcium sensitizers |
| (combination drug containing isosorbide dinitrate and hydralazine) approved only for the treatment of HF in African Americans Hydralazine relaxes arteries and decreases the work of the heart Isosorbide relaxes veins to reduces preload | BiDil |
| most important daily assessment with heart failure | Daily weights are important Same time, same clothing each day Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to health care provider |
| health promotion includes: Treatment or control of underlying heart disease key to preventing HF and ADHF (e.g., valve replacement, control HTN) Antidys agents or pacemakers for those with serious dys or conduction disturb Flu and pneumonia vaccs | heart failure |
| patient education: Medications, taking pulse rate, home BP monitoring, signs of hypo- and hyperkalemia if taking diuretics that deplete or spare potassium | heart failure |
| primary complication cardiac transplantation | infection is the primary complication followed by acute rejection in the first year after transplantation |
| major risk factors associated with PAD | *Cigarette smoking Hyperlipidemia HTN Diabetes Mellitus |
| what is the threat of an AAA | rupture; risk is related to size |
| s/s of posterior AAA rupture | back pain, +/- Grey Turner's sign (bruising of flank) |
| s/s of anterior AAA rupture | massive hemorrhage and hypovolemic shock; decreased LOC, tachycardia, hypotension, decreased urine output |
| major risk factors for AAA | smoking, HTN, emphysema |
| 2 ways an AAA is evaluated | physical exam- palpate abdomen; u/s of abdomen over aorta |
| how fast can an AAA grow once detected | 1/4 cm in diameter per year; higher increase w/ smoking, HTN, emphysema |
| 2 surgical modalities for AAA | conventional open abdomen repair w/ synthetic graft; endovascular approach w/ graft placement passed into aorta from inside |
| follow-up needed for endovascular surgery | check-up every 6 months; imaging study CT every year |
| clinical manifestations include: Sudden severe pain (tearing/stabbing) Anterior chest or intrascapular radiate down spine, abdomen, or legs Neurologic- CVA, paralysis Respiratory- pleural effusion | aortic dissection |
| potentially life-threatening condition in which there is bleeding into and along the wall of the aorta, the major artery leaving the heart | aortic dissection |
| antihypertensive therapy for aortic dissection | IV Beta blocker (ex: esmolol) Calcium channel blocker (ex: Nipride) ACE inhibitors |
| conservative therapy for aortic dissection | Pain management (indication of stabilization) Blood transfusion Treat heart failure |
| surgical therapy for aortic dissection | Preferred treatment for Type A dissection Remove dissected aorta, block the entry of blood, reconstruct aorta (graft/stent) 30 day mortality 10-28% Death r/t MI, cerebral ischemia, uncontrolled bleeding, abdominal ischemia, sepsis, and multi-organ failure |
| perioperative nursing care of a patient having an aortic aneurysm repair | Establish baseline Indications of rupture Assess Family history and cardiovascular risks Patient/family teaching |
| reproducible, exercise induced muscle pain that resolves with rest Femoral/popliteal- calf Aortoiliac- buttocks, thighs, erectile dysfunction | intermittent claudication from PAD of lower extremities |
| Parasthesia- numbness/tingling Feet/toes Neuropathy (DM) Limb appearance Loss of hair, shinny, taut Decreased or absent pedal pulse, popliteal, or femoral Elevation pallor Reactive hyperemia r/t Dependent rubor Rest pain (Critical Leg Ischemia) | clinical manifestations with PAD of lower extremities |
| Lifestyle modification Smoking cessation (no nicotine patch) Treat hyperlipidemia Statins (ex: Zocor) Control DM HbgA1c- <7.0% Control HTN <130/80 | PAD of lower extremities |
| Drug therapy Antiplatelets Ex: ASA (160-325mg), Plavix, Ticlid Treatment for intermittent claudication Trental and Pletal Exercise 30-40 minutes/day; 3-5x/week | PAD of lower extremities |
| Nutritional therapy Low cholesterol Low calorie (in obese patient) Na restriction (2gm/day) | PAD of lower extremities |
| Skin Care Do not soak Prevent cracking Ulcer Clean/dry | PAD of lower extremities |
| Interventional Radiology Percutaneous transluminal balloon angioplasty Stent placement Prevent restenosis | PAD of lower extremities |
| What surgical management can be done for a patient with peripheral arterial disease of the lower extremities? | Peripheral artery bypass with native vein or prosthetic graft (most common) Endarterectomy Patch graft angioplasty Amputation |
| Postoperative care for patient following surgery for PAD of lower extremities | Primary goal each day in patient assessment is confirmation of graft patency; Pulse exam (doppler/palpation), Graft palpation, ABI, Duplex US, Anticoagulation (heparin, lovenox, antiplatelet) Be familiar with surgeons’ incision Minimal drainage Soap/water |
| predisposing risk factors for superficial thrombophlebitis and deep vein thrombosis | Virchow's Triad: venous stasis, endothelial damage, hypercoagulability of blood |
| causes include: Dysfunction of valves Muscles in extremities inactive Obese, atrial fibrillation, long trip, immobile | venous stasis |
| causes include: Trauma or external pressure (venipuncture) IV therapy-worsen damage | endothelial damage |
| causes include: Polycythemia, malignancies, pregnancy Birth control, HRT | hypercoagulability of blood |
| R/t IV therapy, trauma to varicose veins • Pain and tenderness along the vein • Cord-like • Edema of affected extremity • Diagnosed by physical exam • Infectious thrombophlebitis-rare • Febrile • Leukocytosis • +Blood culture | superficial thrombophlebitis |
| +/-Unilateral leg edema • Pain, erythema, warm, febrile (>100.4) • +Homan’s Sign • Pulmonary Embolus • Chronic venous insufficiency • Valvular destruction • edema, ulcerations, cyanosis, Phlegmasia cerulea dolens, Sudden onset, Swollen, blue, painful leg | DVT |
| Treatment • Elevate affected extremity • Warm compress • Remove the IV catheter • Compression stockings (lower extremities) • NSAIDS, ASA | superficial thrombophlebitis |
| Mobilization • BR-change positions, dorsiflex feet q2-4 hours • OOB to chair • Ambulate TID • Antiembolism stockings • Exerts 18 mm Hg pressure • Apply appropriately - Toe hole under toes - No wrinkles - Knee vs thigh high Intermittent Compression Device | DVT prevention/prophylaxis |
| BR, elevate extremity, warm compress, 2-4 days Jobst Stockings (Custom fit 30-40 mm Hg, 3-6 months) Anticoagulation Used for treatment and prophylaxis Vitamin K antag, indirect thrombin inhibitors, direct thrombin inhibitors, and Factor Xa inhibitors | DVT treatment |
| Indication: prevent recurrent PE • Venous thrombectomy • Vena Cava interruption device o Ex: Greenfield filter | venous thrombosis surgical therapy |
| Discomfort along with swelling • Body image disturbance • Pain • Aggravating factor: standing long period • Alleviating factor: walking, elevated limb • Frequent complication- superficial thrombophlebitis • Rare complications: rupture and ulceration | varicose veins |
| Treatment • Sclerotherapy o Reserved for small ones o Wrap ace bandage 24-72hr o Compression stockings 2-3 weeks – Advise long-term use | varicose veins |
| Compression important! • Jobst stockings • Intermittent compression devices • Unna boot • Assess arterial status • ABI • Nutrition (promote wound healing) • Protein • Vitamin A • Vitamin C • Zinc | venous leg ulcers |
| conduction from SA node to just before the impulse leaves the Purkinje fibers | PR interval |
| when the impulse emerges from the Purkinje fibers, ventricular depolarization occurs, producing mechanical contraction of ventricles | QRS complex |
| important in the rate of impulse formation, speed of conduction, & strength of cardiac contraction | autonomic nervous system |
| R & L Vagus nerve causes decreased heart rate, conduction, and irritability (affects atria only) | PNS |
| nervous system that causes increased heart rate, conduction, and irritability (affects atria and ventricles) | SNS |
| electricity flowing toward positive electrode | upright pattern/positive deflection |
| electricity flowing toward negative electrode | inverted pattern/negative deflection |
| a restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue | ischemia |
| process of tissue death (necrosis) caused by blockage of the tissue's blood supply | infarction |
| 0.04 seconds x 0.1 mV | small square |
| 0.20 seconds x 0.5 mV | large square |
| 300 large squares | 1 minute |
| method one: measuring heart rate | a marker appears at top of rhythm strip q 3 secs, thus 2 markers are 6 secs. Count R-R intervals, multiply answer by 10. The sum is the approximate rate per minute. R-wave is first (+) deflection of QRS complex |
| method two: measuring heart rate | Count # of large squares between R intervals then ÷ by 300 |
| atrial depolarization/contraction | P wave |
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