1 nclex rn preparation program cardiovascular disorders module 5, part 2 of 3
TRANSCRIPT
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NCLEX RN Preparation Program
Cardiovascular DisordersModule 5, Part 2 of 3
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Cardiovascular System
IntroductionThe heart and the circulatory
system comprise one
of the most essential
parts of the body.
Failure to function
results in death of
the organism.Photo Source: National Heart, Lung and Blood Institute (NHLBI) http://www.nhlbi.nih.gov/health/dci/Diseases/arr/arr_howheartwork.html
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Gross Structure of the Heart
Layers: Pericardium
Fibrous Serous Pericardium
Epicardium Myocardium Endocardium
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Chambers of the Heart Heart, a muscular organ
divided by a septum into two halves. Right or venous chamber and left or arterial chamber.
Right Chambers Right Atrium Right Ventricle
Left Chambers Left Atrium Left Ventricle
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Coronary Blood Supply Right Coronary
Artery Left Coronary
Artery Left anterior
descending Circumflex
Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program
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Valves of the Heart Valves are strong membranous openings that provide
one-way flow of blood. Atrioventricular valves – prevent backflow of blood
from ventricles to atria during systole. Tricuspid Mitral
Semilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. Pulmonic Aortic
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Valves of the Heart
Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program
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Conduction system Specialized tissue that allows rapid
transmission of electrical impulses through the myocardium
Sinoatrial node – main pacemaker of heart. Normal rhythmic, self-excitatory impulse is generated.
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Conduction system
Photo Source: St. Francis Hospitals & Health Centers, http://www.stfrancishospitals.org/DesktopDefault.aspx?tabid=72&Class=Test&pageid=P07973
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Gross Structure of Vasculature Arteries: transport blood under high
pressure to body tissues Precapillary sphincters Arteriovenous shunts
Capillaries – exchanging fluid and nutrients between blood and interstitial space.
Veins: acts as conduits for transport of the blood from tissues back to heart
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Physiology of the Heart Contraction – shortening or increase in
muscle tension. Utilizes chemical energy to do the work of contraction
Cardiac Muscle Principle: Frank Starling Law: the greater the heart is
filled during diastole, within physiological limits, the greater the quantity of blood pumped into the aorta and pulmonary artery.
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Autonomic Nervous System Control
Cardiac Muscle Sympathetic (Adrenergic) Parasympathetic (Cholinergic)
Systemic blood Vessels Sympathetic – vasoconstriction Parasympathetic – vasodilation
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Baroreceptor Reflex (Pressoreceptors)
Located in the walls of large systemic arteries Rise in pressure results in baroreceptors
transmitting signals to CNS (Central Nervous System) to inhibit sympathetic action
Other signals, in turn, sent to circulatory system to reduce pressure back to normal.
Result: decreased heart rate, vasodilation, decreased BP.
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Other Chemical Controls of Blood Pressure
Kidney Adrenal cortex - aldosterone Renin-angiotensin system
Antidiuretic hormone (vasopressin)
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System AssessmentEvaluate Patient’s History
Pain Dyspnea Cyanosis Fatigue Palpitations Syncope Hemoptysis
Edema Condition of
Extremities
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Evaluate veins and arterial pulses through inspection/palpation
Veins Neck veins Arm and hand veins Leg and foot veins
Arteries Central Peripheral pulses
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Auscultate lung sounds
Lungs Listen for bibasilar crackles – if present,
suspect Congestive Heart Failure (CHF)
Photo Source, Wikimedia Commons, Creative Commons, http://commons.wikimedia.org/wiki/Image:X-ray_lung_consolidation.jpg
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Auscultate heart sounds Heart sounds – frequency, pitch, intensity,
duration Murmurs
Systolic Diastolic
Pericardial friction rubs
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Other parameters to assess
Arterial pressure Carotid blood vessels for bruit Palpate and percuss thorax Evaluate chest x-rays Assess lung sounds
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Diagnostic Tests & Procedures
Laboratory Studies Cardiac Enzymes
CK-MB LDH Troponin Myoglobin BNP
CBC Blood coagulation factors Serum lipids Electrolytes
K, Na
Calcium Phosphorus Magnesium BUN Blood glucose
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Diagnostic Procedures Electrocardiogram Central Venous Monitoring Cardiac Catheterization Echocardiography Angiography Chest x-rays
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Acute Coronary Syndromes
Coronary Artery Disease (CAD) Narrowing or obstruction
of one or more coronary
arteries as a result of
atherosclerosis, an
accumulation of
lipid-containing plaque
in the arteries. Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
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Pathophysiology Atherosclerosis - fat deposited in intima of arterial
wall Inflammatory response begins Macrophages inflitrate area to ingest lipids, then
die Smooth muscles cells within the blood vessel
cover the area with fiber and plaque is formed. If the plaque is thin, the lipid center may grow,
rupture, become a thrombus
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Myocardial Ischemia / Angina Pectoris
Decreased oxygen to heart Exercise-induced chest pain Unstable angina Other risk factors
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Coronary Artery DiseaseMyocardial ischemia
CLINICAL MANIFESTATIONS: May be asymptomatic unless ischemia occurs Chest pains or pressure, may radiate to jaw,
back, shoulder Palpitations, weakness Dyspnea Syncope Nausea Excessive fatigue EKG changes (T wave inversion)
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Coronary Ischemia/Angina
Silent angina - no
symptoms, but
EKG changes.
Often occurs in
diabetic
patients with CAD.
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Teaching for Angina
Rest at onset of chest pain Take one nitroglycerin, repeat 2 more
prn No relief by 3rd, call 911 Previous angina with particular activity,
take nitroglycerin prior to activity
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Unstable Angina Oxygen: 2-4L nasal cannula Nitroglycerin Morphine Aspirin Baseline vital signs 12 lead EKG Monitor for dysrhythmias, heart failure
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Myocardial Infarction
Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
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MI: Signs and Symptoms Pain Nausea Impending doom Diaphoresis Dyspnea Dysrhythmias
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12-lead EKG Normal Ischemia Injury
Acute infarct
Old infarct
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LABS Myoglobin – non specific Troponin CK-MB BNP = CHF
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Collaborative Management Immediate assessment
Vital signs with oxygen saturation 12-lead EKG Cardiac enzymes Chest x-ray Electrolytes – K+ & Mg++
Immediate treatment – “MONA” Beta blockers?
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MONA
Acronym from Advanced Cardiac Life Support (ACLS) though order is ONMA.
O = Oxygen 2-4 liters per nasal cannula N = Nitroglycerin (if not already tried outside
hospital); relieves pain M= Morphine relieves pain, decreases
anxiety, increases venous pooling (to reduce cardiac workload)
A = Aspirin prevents platelet aggregation at the site of obstruction
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Reperfusion Strategies
Thrombolytics Percutaneous
Transluminal Coronary Angioplasty (PTCA)
Stent Procedure
Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
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Post-PCTA Care Monitor V/S Assess distal pulses Bed rest with limb straight for 6 – 8 hours Anticoagulants/antiplatelet agents – prevent
thrombus formation Monitor IV nitroglycerin – prevent coronary
artery spasms ASA once a day permanently Assist planning lifestyle modification
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Acute Myocardial Infarction
Bed rest for 24 to 36 hrs
Pain control
Monitor rhythm
Assess for new murmurs
Monitor potassium, magnesium
Monitor for heart failure
Gradual increase of activities
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Rehabilitation Diet Progressive exercise Change modifiable risk factors
Weight loss Stress reduction Lipid-lowering drugs Anti-hypertensives Aspirin
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Coronary Artery Bypass Graft (CABG)
Bypass grafts sewn from aorta to below area of blockage
Fluid overload Pacemaker? Bleeding Atrial fibrillation
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Nursing Management
Control pain
Early ambulation
Incentive spirometer
Change dressings: watch for infection
Monitor: VS, lungs, heart, weight, I&O, labs, EKG
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Complications Stroke Tamponade: pulsus paradoxus Bleeding Dysrhythmias Post-cardiotomy syndrome
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Cardiac Dysrhythmias
Normal Sinus Rhythm/Regular Sinus Rhythm Rhythm originates from the SA node Atrial and ventricular rhythms are regular Rates are : 60- 100 beats per minute.
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Cardiac Dysrhythmias Sinus bradycardia
Atrial and ventricular rates below 60 beats per minute
Treatment may be necessary if symptomatic Note: low rates may be normal for some
patients.
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A-V block: 2nd Degree Mobitz I
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AV Block: 2nd Degree Mobitz II
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A-V Block: 3rd Degree
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Supraventricular Tachycardia
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Atrial Fibrillation
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Premature Ventricular Contractions (PVCs)
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Ventricular Tachycardia
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Ventricular Fibrillation
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Defibrillation Options
Paddles AED ICD
Photo Source: Wikimedia Commons (Creative Commons), http://commons.wikimedia.org/wiki/Image:Defibrillator_Monitor.jpg
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Asystole/PEA
CPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below:
Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypoglycemia, Hypothermia
Toxins, Tamponade (cardiac); Tension pneumothorax; Thrombosis (coronary or pulmonary); Trauma
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Cardiac Pacemaker
Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the patient’s intrinsic pacemaker fails to provide a perfusing rhythm.
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Pacemakers
Types of Pacemakers Temporary Transvenous invasive temporary pacing Epicardial invasive temporary Permanent
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Patient Education Programmed rate When to notify MD:
Dizziness, weakness, sudden weight gain of 3-5 pounds overnight, persistent hiccups. Check pulse daily, report sudden slowing or increasing of pulse.
Signs/symptoms to report:Fever, redness, swelling, drainage from insertion site, dizziness, fatigue, shortness of breath, chest pains, swelling of ankles/legs
Pacemaker identification, medic alert Measure pulse daily, keep record
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Patient Education(continued)
Wear loose-fitting clothing Avoid contact sports Inform all health care providers of pacemaker Most electrical appliances can be used
without any interference with the functioning of the pacemaker.
If any unusual feelings occur when near any electrical devices, move 5 to 10 feet away and check pulse.
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Congestive Heart Failure Inability of the heart to maintain adequate
circulation to meet the metabolic needs of the body because of impaired pumping actions.
Cardiac output diminished and peripheral tissue not adequately perfused
Congestion of the lungs and periphery may occur.
Classification: Acute and Chronic Types: Right-sided/left-sided heart failures
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Congestive Heart Failure Clinical manifestations
Weight gain, I & 0, edema, if severe: ascites Crackles in lungs (especially bibasilar) Dyspnea, orthopnea, urinary frequency, murmurs (if valve problem) S3 heart sound - sign heart beginning to fail & increased
blood volume remains in heart after each beat BNP lab test - the higher the number, the worse the CHF
is. Can monitor severity of CHF, improvement due to treatment regimen, timely diagnosing of CHF
Jugular vein distension, LOC, pulse oximetry.
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CHF: Collaborative Mgmt
Vasodilators: Nitrates Positive inotropes: increase contraction
Digoxin (Lanoxin) Beta blockers (though some
contractility & are contraindicated) ACE inhibitors
Diuretics
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CHF: Nursing Management Elevate head of bed Give oxygen Decrease oxygen demand Exacerbation? Identify precipitating factors Teach: low-salt diet, medications and their
rationale, weigh daily, exercise but pace activities. Wait 90 min. after meals to exercise. Avoid extremes in weather when exercising.
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Cardiac Valve Disorders
Mitral stenosis
Mitral prolapse
Aortic stenosis
Aortic regurgitation
Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
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Cardiac Valve Disorders
Clinical Manifestations: Heart murmur Left ventricular hypertrophy seen on EKG
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Congestive Heart Failure
Photo Source: Lippincott, Williams, & Wilkins Connection Image Bank, http://connection.lww.com/products/smeltzer9e/imagebank.asp
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Congestive Heart Failure Collaborative Management
Digoxin (inotropic) Diuretics (lasix, aldactone) Coreg - beta blocker shown to improve
cardiac function in CHF patient Ace inhibitor - shown to improve cardiac
function in CHF patient Oxygen, cardiac rehab
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CHF Management (continued)
Treat heart failure if present Atrial fibrillation? Antibiotic prophylaxis Weigh daily
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Pericarditis
Inflammation of pericardial sac. Can be caused by viral infection, complicaton after cardiac surgery 10 days to 2 months, or after MI
Idiopathic cause, or disorder of connective tissue (lupus), cancer, radiation therapy, etc
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Pericarditis: Manifestations
Chest pain on inspiration, worse when patient leans forward, lying down or turning
Pericardial friction rub Symptoms of right-sided heart failure Mild fever, elevated WBC, ESR Atrial fibrillation common 12 lead EKG may have elevation in ALL leads Can worsen to cardiac tamponade
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Pericarditis Collaborative Management
NSAIDs or corticosteroids Pericardiocentesis or surgical pericardial
window
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Pericarditis: Nursing Mgmt Position for comfort Monitor for cardiac tamponade (fluid between
heart and pericardial sac) that causes heart to be compressed inside the sac leading to decreased blood pressure and shock, distant heart sounds
Teach: gradual increases of activity Teach: avoid aspirin, anticoagulants
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Infective Endocarditis Valves infected, spreads to endothelium Leaflets deform, leak High risk: elderly, prosthetic valves, IV
drug abusers, immunosuppressed
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Manifestations Slow onset
Flu-like symptoms, anorexia, weight loss, joint & back pain, fever, splinter hemorrhages undernails, petechiae, murmur, headache?
Major complication: embolus Diagnosis: blood culture, echocardiogram
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Management IV antimicrobials based on cultures Teach prevention Monitor: sepsis, new murmur, stroke,
meningitis, CHF
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Hypertension Pathophysiology
90-95% unknown cause 5-10% secondary causes Some genetic tendency, obesity, stress,
excess sodium intake Prolonged hypertension eventually damages
blood vessels, heart (LVH) and kidneys, eyes, brain.
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Hypertension Clinical manifestations
Usually asymptomatic “silent killer” Some report headache, especially early morning
Risk factors Family history Age Diabetes Obesity Heavy alcohol High sodium intake
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Hypertension Goals: reduce BP. Goal: 120/80 Ask for S/S indicative of HTN Obtain BP on both arms Family history, weight, dietary patterns Identify medication therapy Assess cardiac, neuro, renal, diagnostic
and lab studies.
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Hypertension Collaborative Management
Medications: diuretics, beta blockers, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockers
Monitor and routine follow-up with EKG, lipid lower agents if needed
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Hypertension Nursing Management
TEACH: weight loss, stress management, rationale for medications prescribed & their importance. Low-sodium, low-fat, low-cholesterol diet. Stop smoking. Limit caffeine, alcohol. Teach how to modify risk factors.
Monitor for target-organ problems. Teach potential problems if hypertension untreated.
Many people undiagnosed. Promote screening for early detection.
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Classification
Category Systolic Diastolic
Normal <120 mmHg <80 mmHg
Pre-HTN 120-139 or 80-89
Stage 1 140-159 or 90-99
Stage 2 ≥ 160 or ≥ 100
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Hypertensive Crisis…Assessment
Diastolic pressure > 120 mm Hg. Headache Drowsiness Confusion Changes in LOC Tachycardia and tachypnea Dyspnea/cyanosis/seizure
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Hypertensive Crisis: Mgmt Lower BP slowly
IV nitrates (nitroglycerin) Nitroprusside (Nipride) Enalapril (Vasotec) Beta blockers Diuretics
Monitor rhythm, vital signs
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Peripheral Vascular Disease (PVD)
Pathophysiology Generalized atherosclerosis (plaque
development) or arteriosclerosis (hardening of the arteries)
Narrowing of lumen, obstruction by thrombosis
Bifurcation or branch areas higher risk of blockage.
If have PVD, at risk of having CAD as well
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Peripheral Arterial Disease
Stage I: Asymptomatic Stage II: Claudication Stage III: Rest pain Stage IV: Necrosis
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PVD: Management Medications Control hypertension Angioplasty, bypasses Exercises Position Vasodilation Avoid vasoconstriction
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Arterial Bypass
Monitor for graft occlusion Promote graft patency Monitor for compartment syndrome
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Peripheral Venous Insufficiency
Stasis dermatitis lower legs Edema Ulcers over malleoli Anterior leg ulcers if arterial flow
impaired
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Peripheral Vascular Disease Compression stockings Sequential compression pump Manage ulcers Elevate legs Avoid prolonged sitting or standing No compression of legs
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Abdominal Aortic Aneurysm
Localized dilatation of the wall of the abdominal aorta caused by congenital weakness, trauma, disease, atherosclerosis
Risk factors: smoking, hypertension Progressive weakening and enlarging of area of vessel If a tear develops - medical emergency (rupture)
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Aortic Aneurysms Goal of treatment:
limit progression of the condition by modifying risk factors, controlling BP, recognizing symptoms early, and preventing rupture
Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
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Abdominal Aortic Aneurysm Clinical Manifestations:
Can palpate enlarged aorta, possible bruit ausculated
If rupture, sudden pain in back or abdomen
If tearing, pain in abdominal area or back; can be slowly progressive
If rupture-hemorrhage, shock, death unless emergent surgical intervention
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Manage Abdominal Aneurysm
Non-surgical:
Modify risk factors Monitor BP Regular exams for size, pulsation Report: chest/back pain, SOB, Difficulty
swallowing, hoarseness
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Thoracic Aortic Aneurysm
Pain: neck, shoulders, lower back or abdomen
Syncope Dyspnea Tachycardia Cyanosis Weakness
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Manage Thoracic Aneurysm Monitor V/S Assess for pain – abdominal or back
pains. Check peripheral pulses, including
temperature and color Observe for signs of rupture Note tenderness/distention of abdomen
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Photo Acknowledgement:All unmarked photos and clip art
contained in this module were obtained from the
2003 Microsoft Office Clip Art Gallery.