Common Cardiovascular Problems
NUR 475 – Family Nurse Practitioner III
Common Cardiovascular and Peripheral Vascular Problems – Part 2
Prevention, early identification and effective treatment significantly reduces
cardiovascular morbidity and mortality
Nurse Practitioners must focus on health maintenance and disease prevention, as well as
diagnosis and management of disease. This includes a focus on the foundations of health.
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A healthy diet
Regular physical exercise (not just activity)
Good quality and quantity of sleep
Good hygiene
Common Chief Complaints
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Chest pain
Palpitations
Dizziness
Fatigue
Lower extremity swelling
Common Cardiovascular disorders
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HTN - Hypertension
Hyperlipidemia
CAD - Coronary Artery Disease
ACS – Acute Coronary Syndrome
MI – Myocardial Infarction
Syncope
AF - Atrial Fibrillation
Cardiac valve
Endocarditis – bacterial prophylaxis
Cardiomyopathy
CHF – Congestive Heart Failure
Common Peripheral Vascular disorders
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Arterial
Venous
1
Common Cardiovascular Problems
2
Atrial fibrillation
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Clinical guidelines Clinical guidelines
http://circ.ahajournals.org/content/114/7/700.full.pdf+html and
http://circ.ahajournals.org/content/123/1/104.full.pdf
Most common cardiac dysrhythmia - ↑ incidence and prevalence with aging
Pathogenesis
o May be precipitated by trauma, obstructive sleep apnea, pericarditis, chest surgery,
thyroid disorders, pulmonary disease, drugs, alcohol excess/withdrawal
o 5-fold increased risk of stroke
Symptoms
o Palpitations (acute onset)
o Fatigue (chronic)
Signs
o Irregular and often tachycardic heart beat
o High rate can lead to hypotension, myocardial ischemia and dysfunction
o Pulse deficit
Diagnostic testing
o ECG – fast and irregular atrial rate, variable ventricular response
o Chest x-ray (pulmonary disorder?)
o Doppler echocardiogram (valvular disease, LVH)
o In selected cases - TSH/T3/T4, CBC, CMP, polysomnogram
Treatment – 3 objectives (rate control, prevention of thromboembolism, and correction of the
rhythm disturbance)
o Prevention of thromboembolism - Anticoagulation
 Warfarin or dabigatran (Pradaxa) – lower risk of major bleeding, no dietary
restrictions, no regular INR, drug-drug interactions unlikely, more GI side effects, not
for valvular disease
(1) See: Outpatient management of Anticoagulation Therapy at
http://www.aafp.org/afp/2007/0401/p1031.html
(2) See Warfarin Therapy: Evolving Strategies in Anticoagulation at
http://www.aafp.org/afp/1999/0201/p635.html?printable=afp
 Aspirin and clopidogrel
o Rate control, rhythm correction
 Goal of rhythm <110 bpm
 β blocker, verapamil, diltiazem or digoxin
 amiodarone versus dronedarone (Multaq)
 Cardioversion for new onset; in selected cases for chronic after anticoagulation
 Catheter ablation in selected patients
Referral
o Hospitalize when hemodynamically compromised
o Symptomatic with or without rate control
o Poor rate control
Case study #8 (in class) - notes
Common Cardiovascular Problems
Cardiac valve disorders
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Regurgitation/insufficiency
o Retrograde (backward) flow of blood “upstream” when the valve should be closed
Stenosis
o Obstruction of the (forward) flow of blood across an open valve
S1=closing of atriovenricular valves (mitral and tricuspid)
S2= closing of semilunar valves (aortic and pulmonic)
Murmurs graded I-VI
Systolic murmurs
o Aortic stenosis
 S&S; syncope, angina and dyspnea on exertion
 Associated findings; rales in lung bases with LVH, JVD, hepatomegaly, peripheral
edema with RVH
o Pulmonic stenosis (more common in women)
 More common in women
 Often hemodynamically insignificant
 S&S; dyspnea, cyanosis, syncope on exertion, palpitations, right heart failure
o Hypertrophic cardiomyopathy or idiopathic hypertrophic subaortic stenosis
 Cause unknown, may be genetic
 S&S; dyspnea on exertion, chest pain, syncope (during or after exercise), atrial
fibrillation, AND
 Ventricular dysrhythmias causing sudden death especially after exertion –
important with athletic screening →
 What history should be obtained and documented?
 What physical examination should be done and documented?
o Mitral regurgitation
 S&S; dyspnea and palpitations most common, atrial fibrillation
 Bacterial endocarditis concern
o Mitral valve prolapse
 10% of young women, generally hemodynamically insignificant
 S&S; usually asymptomatic, palpitations
 Bacterial endocarditis concern
o Tricuspid regurgitation
 Common with pulmonary hypertension and LVF
 S&S; fatigue, abdominal and ankle swelling, ascites, liver congestion, atrial
fibrillation
o Physiologic or functional murmurs
 Temporary increase in blood flow due to anemia, hyperthyroidism, pregnancy and
fever
o Innocent murmurs
 Commonly occur in children and young adults
 Caused by turbulent blood flow due to great velocity of flow during early systole
Diastolic murmurs – almost always pathologic!
o Mitral stenosis
 S&S; dyspnea on exertion, hemoptysis, rales, orthopnea, atrial fibrillation
3
Common Cardiovascular Problems
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o Tricuspid stenosis
 Often caused by rheumatic fever
 S&S; fatigue, right upper quadrant discomfort (enlarged liver)
o Aortic insufficiency/regurgitation
 Life threatening → acute pulmonary edema (dyspnea, orthopnea, cough)
 Most common cause is infective endocarditis with rheumatic fever
 Chronic S&S; palpitations possibly due to ventricular dysrhythmias, dyspnea and
chest pain (LVH), diaphoresis
o Pulmonic insufficiency/regurgitation
 Often in pulmonary hypertension and LVH
 S&S; cor pulmonale, dyspnea on exertion
o Ventricular septal defect
 Congenital
 Left-to-right shunting causes increased blood flow over pulmonic valve
 Large defects - dyspnea on exertion
o Atrial septal defect
 Congenital
 Left-to-right shunting causes increased blood flow over tricuspid valve to the lungs
 S&S; asymptomatic until early adulthood then dyspnea on exertion, palpitations,
atrial dysrhythmias, RHF
Diagnostic testing
o Chest X-ray – enlarged ventricles
o ECG – dysrhythmias
o Echocardiogram – valve disease
o Cardiac catheterization – unstable, surgical intervention
Case study # 9 (in class) – notes
Bacterial endocarditis prophylaxis
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See clinical practice guidelines http://circ.ahajournals.org/content/116/15/1736.full.pdf
Used in what 2 conditions?
4
Common Cardiovascular Problems
Pericarditis
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Case study #10 (in class) – notes
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First must rule out MI and cardiac tamponade (serious complication requiring urgent
pericardiocentesis)
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Essential Evaluation:
o Detailed symptom description and relevant history
o Vital signs including temperature
o Chest and cardiac examination
o ECG
 electrical alternans with tamponade
 diffuse ST ↑ and associated PR depression
o If suspect MI
 Cardiac biomarkers
o If suspect pericarditis
 CBC (↑ leukocytes), ESR (↑)
 Chest x-ray (normal or effusion and ↑ cardiac shadow)
Pathogenesis
o Acute pericarditis (inflammation for 1-2 weeks)
 5% of non-ischemic chest pain
 Idiopathic in most cases, presumed viral
 Dressler syndrome – 24-72 hours after transmural MI
 Chest trauma (including post coronary artery by-pass surgery)
o Constrictive pericarditis (occurs over time due to scarring of pericardial sac from a
disease processes)
 Connective tissue disorders (rheumatoid arthritis, SLE, scleroderma, sarcoidosis)
 Bacterial, viral or fungal infections including HIV and TB
 Chest trauma (including post coronary artery by-pass surgery, AICD pads)
 Neoplastic
 Uremia
 Irradiation
 Idiopathic
S&S
o Sharp, stabbing, crushing, steady anterior chest pain
o Pain worsens with inspiration, lying flat or leaning forward
o May be associated with shortness of breath, fever, chills and malaise
o Additionally in constrictive pericarditis
 S&S of RHF and low cardiac output
 Lower extremity edema
 Abdominal complaints
 Hepatic congestion, possibly jaundice
 Atrial fibrillation
 Tricuspid regurgitation
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Common Cardiovascular Problems
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Differential Diagnosis; see chest pain section
Differentiation of Acute Pericarditis from Myocardial Ischemia or Infarction
Clinical finding
Acute Pericarditis
M. Ischemia or Infarct
Chest pain
Character
Duration
*Change with position
Change with respirations
Response to nitroglycerin
Electrocardiography
P-R segment depression
Q waves
Ration of ST-segment
elevation to T-wave
amplitude in V6
ST-segment elevation
No change
T waves
Inverted after ST segments
have normalized
Inverted when ST segments
are still elevated
*Friction rub on physical
exam
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Physical Examination
o Pericardial friction rub in 60-70%
o In constrictive pericarditis
 Marked JVD
 Kussmaul sign
 Pericardial knock
 Hepatomegaly
 Spider angiomata
 Palmar erythema
Additional diagnostic testing
o Echocardiogram
o CT or MRI if workup inconclusive-consult cardiology
Treatment (Goal is to relieve pain and prevent complications. Most cases are uncomplicated
and can be managed in outpatient setting.)
o Acute pericarditis
 Focus on cause
Common Cardiovascular Problems
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NSAIDS (ibuprofen 600-800 mg 3 times a day for 2 weeks); can use aspirin, avoid
Indocin especially in elderly (↓ coronary flow)
 Colchicine - 2-3 mg loading dose followed by 1 mg daily for 10-14 days
 Corticosteroid – for unresponsive cases only, (can cause relapse); 60 mg for 2 days
and taper over 7 days
o Chronic pericarditis
 Corticosteroids may be helpful
 Pericardiectomy
 Diuretics and sodium restriction with RHF
 Avoid β blockers and calcium antagonists (HR of 80-90 bpm acceptable, use Digoxin
in atrial fibrillation first)
 Hospitalize for acute pericarditis for
o Cardiac tamponade
o Body temperature control
o Anticoagulation therapy
o Surgical treatment
o Immunocompromised
 Case study # 11 (in class) – notes
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Cardiomyopathies
Dilated
o Most common
o 50% idiopathic
Hypertrophic (HCM) previously known as hypertrophic obstructive cardiomyopathy
and idiopathic hypertrophic subaortic stenosis
o Resource: http://www.mayoclinic.com/health/hypertrophiccardiomyopathy/DS00948
o Prevalence 1:500
o Mutation of 10 genes coding protein of the cardiac sarcomere
o Slight male predominance up to mid-life; female predominance over 60 years of
age
o Inappropriate and marked left ventricular hypertrophy, ranging from mild to
extreme, esp. localized hypertrophy, typically in the anterior septum. This
hypertrophy may result in areas of ischemia or infarction due to abnormal
microvasculature, impaired coronary vasodilator reserve, or mismatch between
myocardial mass and coronary circulation. This causes scarring.
o Outflow tract obstruction, not demonstrated in the majority; causes a loud systolic
murmur and may be symptomatic with exertion intolerance, syncope, or sudden
death
o Highest predictors of sudden death – marked LVH, abnormal BP response to
exercise, syncope, history of cardiac arrest, documented sustained
ventricular tachyarrhythmia and family history of sudden death
Restrictive
o Less common
o 50% due to noninfiltrative (familial, diabetic, others) and infiltrative (amyloidosis,
sarcoidosis, others)
Common Cardiovascular Problems
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 Arrythmogenic right ventricular
 Unclassified
S&S of HCM
 Majority asymptomatic or have mild symptoms
 Dyspnea, chest pain, presyncope or syncope with symptoms worse with exertion
 Primarily related to diastolic dysfunction
 Atrial fibrillation occurs in ¼ of patients thus hemodynamic compromise because of
inadequate filling of the hypertrophied ventricle.
Physical Examination for HCM
 Forceful and enlarged precordial impulse, often laterally displaced
 Murmur results from flow through the left ventricular outflow tract, and is usually a harsh
crescendo-decrescendo, starts well after the first heart sound and is best heard between
the apex and left sterna border. The murmur increases with maneuvers that increase the
gradient through increased contractility, decreased preload, or decreased afterload;
conversely, the murmur decreases with interventions that decrease contractility, increase
preload or increase afterload.
i) Squatting (increased afterload) = decreased murmur
ii) Standing (decreased afterload) = increased murmur
iii) Valsalva (decreased preload) = increased murmur
iv) Precordial impulse-presystolic, systolic, and late systolic impulse (“triple ripple”)
Diagnostic testing for HCM
 Echocardiogram – examines outflow tract obstruction, septal hypertrophy which is
usually asymmetric, and enhanced contractility. Systolic anterior motion of the anterior
mitral valve is present if there is outflow tract obstruction.
 ECG – LVH, prominent Q waves in the inferior and lateral leads due to septal
hypertrophy. Giant negative T waves suggest the apical variant of HCM
 Stress testing
Treatment for HCM
 β blockers are considered the initial therapy of choice
 AICD if considered high risk for sudden death
Heart Failure
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Case study #12 (in class) – notes
Epidemiology
o Increasing incidence and prevalence ~ 5000,000 new cases/year
o > 75% of new and existing cases in 65 and over age group
Pathogenesis
o Normal → injury → compensatory hypertrophy (remodeling) → dilated and fibrotic
(distorted architecture)
o Impaired ability of ventricles to fill or eject blood
o Circulatory and neurohormal response (SNS, RAAS) to cardiac dysfunction
o Systolic dysfunction; inability of the left ventricle to pump blood to the body
 Ejection fraction less than 40%
 Myocardial contractility
 Heart rate (↓ SV → ↑ HR → ↓ CO = HF)
Common Cardiovascular Problems
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 Preload (end-diastolic volume or pressure)
 Afterload (ventricular wall tension during systole → ejection from left ventricle)
o Diastolic dysfunction; inability of left ventricle to relax and fill normally
o Risk factors: Physical inactivity, BMI ≥ 30, excessive alcohol intake, smoking, high
sodium intake
Symptoms
o LV failure
 Exertional dyspnea → orthopnea → paroxysmal nocturnal dyspnea → at rest
 Others; fatigue, cough, nocturia
o RV failure
 Peripheral edema, loss of appetite, nausea
 Often LV symptoms
Signs
o LVF – S3, rales
o RVF – S4, JVD, peripheral edema, hepatomegaly, acites
o In many cases no specific signs
Differential Diagnosis
o Underlying causes; CAD (“plumbing”), HTN, cardiomyopathies, valvular disease
(“structure”), dysrhythmias (“electrical”)
o Precipitating factors; MI, PE, exacerbation of HTN or COPD, infections, drugs, etc.
o Non cardiac: pulmonary disease, thyroid abnormalities, hemoglobinopathies, renal
dysfunction, obstructive sleep apnea, inflammatory disorders, metabolic disorders, drugs
and toxins
o Other causes of peripheral edema
Diagnostic testing
o Chest x-ray
o Brain natriuretic peptide (BNP) – specific to ventricular stretch and correlated with
severity
o Echocardiogram
Treatment
o Acute
 IV loop diuretics and vasodilators
o Chronic management – see Clinical guideline at
http://www.annals.org/content/155/4/252.full.pdf+html
 First line: ACE-I and β-blocker or ARB if intolerant to ACE-I
Referral – hospitalize when unable to manage symptoms in the office/home
o Requires IV drug therapy, oxygen
Follow-up and prevention
o Proper medication use
o Guided exercise
o Smoking cessation
o Weight reduction
o Immunization; flu and pneumonia
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Common Cardiovascular Problems
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Common Peripheral Vascular disorders
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Occlusive or inflammatory disease in the peripheral arteries, veins or lymphatics.
Differentiation of Arterial and Venous Insufficiency
Sign
Pulse
Edema
Pain
Temperature
Color
Arterial Insufficiency
Venous Insufficiency
Decreased/absent
Normal
Absent or mild
Significant
Severe
Absent/mild
Cool
Normal
Pallor with elevation; dusky red on
Hyperpigmentation; cyanotic on
dependency
dependency
Skin
Thin, atrophic; risk of gangrene
Thick; risk of stasis ulcer
Goolsby, M. J. & Grubbs, L. (2011). Advanced assessment: interpreting findings and
formulating differential diagnosis (2nd Ed.). F.A. Davis: Philadelphia, PA.
Arterial Disease
Arterial Insufficiency (PAD, LEAD)
See clinical guidelines at
http://content.onlinejacc.org/article.aspx?articleid=1146931&resultClick=1
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Epidemiology
o Symptoms of lower extremity arterial insufficiency are common in old age.
o Affects 12-20% of people older than age 65
o Affects 8-12 million individuals of all ages in the United States
o Age 65-74: Highest rate of newly sx. LEAD– Lower Extremity Arterial Disease
o In middle age, affects men 2X > women
o Gender disparity begins to disappear after age 65
Pathogenesis
o Refers to any occlusive process that limits blood flow to limbs or to vital organs other
than the heart
o Underlying atherosclerosis
o Most often due to enlarging atherosclerotic plaques in the distal aorta and its branches
o Rarely confined to the lower extremities…By the time lower limb ischemia is
symptomatic, cerebrovascular disease and CAD are usually present as well.
o Risk factors (same as CAD); DM, HTN, Obesity, age, hyperlipidemia, tobacco use
S&S
o Initially, may be asymptomatic, progresses to intermittent, and for some then severe
ischemic pain
o Rapid onset of pain, often described as cramping with activity
o Aortoiliac disease – pain in buttocks or thigh muscle
o Femoral or popliteal diseases – pain in calf muscle
o Relief from pain with rest (intermittent claudication)
3 Clinical Presentations of LEAD
o Young smoking man, age 40-60, with hyperlipidemia & family hx. of vascular disease
Common Cardiovascular Problems
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o Man or woman age 65-75 who c/o calf aching or burning
o Diabetic patient of either sex, with years of suboptimal control
Differential Diagnosis
o Venous insufficiency
o Peripheral neuropathy
o DJD of lumbar spine
Physical Examination
o General; hair distribution, nails, muscle bulk
o CV
o Lower extremity vascular exam
o Diminished or absent pulses
o Blanching with limb elevation
o Dependent rubor
o Decreased distal skin temperature
o Ulcer’s (tissue loss)
o Lower extremity neurological exam
o DTRs
o Sensation
o Strength
Diagnostic testing
o ABI (Ankle-Brachial Index)
o Normal 1.00 or higher
o < 0.5 = impaired flow → vascular consult
Treatment
o Daily exercise
o Foot care
o Treat hypercholesterolemia, HTN and DM
o No smoking
o Debridement of ulcers
o Antiplatelet therapy (aspirin, clopidogrel)
o Pentoxifyline or cilostazol, is selected cases
o Arterial reconstructive surgery
o Percutaneous transluminal angioplasty or stent
Raynaud’s phenomenon
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Usually benign, may have underlying disorder (see Faci page 740)
S&S
o Fingers blanch, next cyanotic, then red with cold exposure
Treatment
o Keep hands warm
o CCB or α-adrenergic antagonists, may be helpful
Case study # 13 (in class) – notes
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Common Cardiovascular Problems
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Venous Disease
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Varicose veins – see readings
Superficial Thrombophlebitis – see readings
Deep Venous Thrombosis (DVT) - See clinical guidelines:
o Management of venous thrombolembolism:
http://annals.org/article.aspx?articleid=732701
 What are the usual causes of VTE (venous thromboembolism)?
 What might be the etiology if it is an “idiopathic” VTE?
 Post-thrombotic syndrome: What is this?
Chronic Venous Insufficiency (CVI)
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Essentials Features
o History of prior DVT or leg injury
o Edema, stasis (brawny) skin pigmentation, subcutaneous liposclerosis in the lower leg
o Large ulcerations at or above the ankle are common (stasis ulcers)
Epidemiology
o One quarter to a third of all adults in western world have varicose veins
o USA-80 million; estimates of the prevalence 7-60% of adults; Best point estimate is 30%
o 1 million-venous ulceration due to venous incompetence of superficial system
o 100,000 disabled
Pathogenesis
o Chronic elevation in venous pressure; normally can hold large volume changes that can
occur with exercise; when valves in the deep or perforating veins are destroyed as in
thrombophlebitis, valvular reflux and bidirectional flow result in high ambulatory venous
pressures. Damage to any component of the calf muscle pump can cause dysfunction of
the pump, thus leading to superficial varicosities, edema, fibrosis of the subq tissue and
skin, hyperpigmentation, and later, dermatitis and ulceration.
o Long-term complication of venous thrombosis due to destruction of deep vein valves
o Potentially life-threatening complication → thrombophlebitis leading to pulmonary
emboli
o Frequently caused by varicose veins
o Often secondary to DVT
o Other causes; trauma, pelvic neoplasm, immobilization, pregnancy
S&S
o Gradual onset of aching, heaviness, tiredness, cramps, itching, burning, restlessness or
pain in lower leg for hours to days
o Question about prolonged immobility or travel
o See the following website for pictures of common findings:
http://www.veinclinics.com/cme/skin-findings.html
Common Cardiovascular Problems
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Differential Diagnosis
o DVT
o PAD
o Peripheral neuropathy
o Lymphedema
 Associated with brawny thickening in the subcutaneous tissue that does not respond
to elevation; edema is particularly prominent on the dorsum of the feet, and in the
toes (sausage toe); varicosities are absent, often history of recurrent cellulitis
o Heart Failure
o Chronic Renal Failure
Physical Examination
o Pulses
o Ankle edema - earliest sign
 Check groin to ankle
 Unlike the edema associated with salt-retaining conditions such as heart failure and
nephrotic syndrome, the edema that precedes venous ulcer formation accumulate
under high pressure, creating tissue damage that is tender.
o Thinning and hyperpigmentation of skin
Common Cardiovascular Problems
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Hyperpigmentation-hemoglobin deposited in the tissues is digested, but the iron
remains in the dermis as hemosiderin and produces a brown or brown-red
pigmentation in skin surrounding ulcer
 Stasis Dermatitis-DeGowin-increased venous and capillary pressures lead to
inflammation, edema, subcutaneous fibrosis, and skin atrophy with hemosiderin
staining. Often mistaken for cellulitis. With chronic disease, the subcutaneous tissues
become fibrotic and the edema no longer pits (brawny edema).
o Superficial veins and varicosities
 Include inspection of abdomen
 telangiectatic veins
o Venous stasis
o Ulcers
o Lower extremity neurological exam
 Proximal and distal strength
 Sensory exam; particularly to sharp and dull
 Deep tendon reflexes
 Casual, toe, heel and tandem gaits
Interesting cases
o Lipodermatosclerosis-“Champagne bottle” appearance- leg assumes the shape of an
inverted champagne bottle – wide at knee narrow at the ankle)
o Eczema to ulceration - case study of Mr. Crabbe:
http://www.worldwidewounds.com/2005/november/Doherty/Encourage-patientInvolvement-Mgt-Lymphovenous.html
o Review website for pictures of ulcers at
http://www.bmj.com/cgi/content/full/320/7249/1589
Diagnostic testing
o Duplex Doppler ultrasound – accurate for clots in large vessels not small thrombi
 Not needed with intact skin and normal pulses
o Venography – most accurate
o MRI – if ulcer and considering osteomyelitis
o Labs to rule out autoimmune/blood disorders
Treatment
o Prompt treatment for DVT with anticoagulants ↓ risk
o Elevation of legs intermittently during the day and at night
o Avoidance of prolonged sitting or standing
Common Cardiovascular Problems
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o Support or compression stockings (TEDs not enough pressure)
 If ulcer present use the Rule of 6, see below
Compression Strength
8-15mm
15-20mm
20-30mm
30-40mm
40-50, 50-60 mm
Indications
Leg fatigue, mild swelling, stylish
Mild aching, swelling, stylish
Requires prescription-Aching, pain, swelling,
mild varicose veins
Requires prescription-Aching, pain, swelling,
varicose veins, post-ulcer
Requires prescription-Recurrent ulceration,
lymphedema
o
o
o
o
o
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Unna boot for stasis ulcers
Pentoxifylline may be helpful (consider drug/drug interactions)
Sclerotherapy
Ambulatory phlebectomy
Procedures, see http://www.veindirectory.org/content/surgical_methods.asp
 Endovenous ablation with laser or radiofrequency-video
 Subfascial endoscopic perforator surgery (SEPS)
 Transilluminated Power Phlebectomy (TIPP)
 Surgical vein ligation or stripping
Refer for non-healing venous ulcers, arterial ulcers and neuro/DM
Location
Lesion features
Surrounding skin
Palpation findings
Comparison of 3 common types of leg ulcers
Venous
Arterial
Neuro/DM
Garter area of leg-will
Pressure sites/toes,
Pressure sites/plantar,
break down/medial
heels, foot
arches heels, toes
leg
Shallow, partial
Punched-out, eschar
Punched-out
thickness with
(blackened if necrotic)
irregular
borders/shaggy
Hyperpigmented,
Hair low, not
Hair loss, not
thickened, with
hyperpigmented,
hyperpigmented,
dermatitis-stasis
atrophic
callus
changes
Non-pitting, tight
Peripheral pulses
Altered sensation with
edema; peripheral
decreased, capillary
touch, vibration,
pulses may be normal
refill time increased
peripheral pulses
decreased