Common Cardiovascular Problems 1

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.

A healthy diet Regular physical exercise (not just activity) Good quality and quantity of sleep Good hygiene

Common Chief Complaints

Chest pain Palpitations Dizziness Fatigue Lower extremity swelling

Common Cardiovascular disorders

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

Arterial Venous

Common Cardiovascular Problems 2

Atrial fibrillation

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)

Signso Irregular and often tachycardic heart beato High rate can lead to hypotension, myocardial ischemia and dysfunctiono Pulse deficit

Diagnostic testingo ECG – fast and irregular atrial rate, variable ventricular responseo 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

Referralo Hospitalize when hemodynamically compromisedo Symptomatic with or without rate controlo Poor rate control

Case study #8 (in class) - notes

Common Cardiovascular Problems 3

Cardiac valve disorders

Regurgitation/insufficiencyo Retrograde (backward) flow of blood “upstream” when the valve should be closed

Stenosiso 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 RVHo 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

fibrillationo 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!

Common Cardiovascular Problems 4

o Mitral stenosis S&S; dyspnea on exertion, hemoptysis, rales, orthopnea, atrial fibrillation

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), diaphoresiso 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 ventricleso ECG – dysrhythmiaso Echocardiogram – valve diseaseo Cardiac catheterization – unstable, surgical intervention

Case study # 9 (in class) – notes

Bacterial endocarditis prophylaxis

See clinical practice guidelines http://circ.ahajournals.org/content/116/15/1736.full.pdf Used in what 2 conditions?

Common Cardiovascular Problems 5

Pericarditis

Case study #10 (in class) – notes

First must rule out MI and cardiac tamponade (serious complication requiring urgent pericardiocentesis)

Essential Evaluation:o Detailed symptom description and relevant historyo Vital signs including temperatureo Chest and cardiac examinationo 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)

Pathogenesiso 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 & So Sharp, stabbing, crushing, steady anterior chest paino Pain worsens with inspiration, lying flat or leaning forwardo May be associated with shortness of breath, fever, chills and malaiseo 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

Common Cardiovascular Problems 6

Differential Diagnosis; see chest pain section

Differentiation of Acute Pericarditis from Myocardial Ischemia or InfarctionClinical finding Acute Pericarditis M. Ischemia or InfarctChest pain Character Duration

*Change with position

Change with respirations

Response to nitroglycerin No changeElectrocardiography P-R segment depressionQ wavesRation of ST-segment elevation to T-wave amplitude in V6ST-segment elevation

T waves Inverted after ST segments have normalized

Inverted when ST segments are still elevated

*Friction rub on physical exam

Physical Examinationo Pericardial friction rub in 60-70%o In constrictive pericarditis

Marked JVD Kussmaul sign Pericardial knock Hepatomegaly Spider angiomata Palmar erythema

Additional diagnostic testingo Echocardiogramo 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 7

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 dayso 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 tamponadeo Body temperature controlo Anticoagulation therapyo Surgical treatmento Immunocompromised

Case study # 11 (in class) – notes

Cardiomyopathies Dilated

o Most commono 50% idiopathic

Hypertrophic (HCM) previously known as hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis

o Resource: http://www.mayoclinic.com/health/hypertrophic-cardiomyopathy/DS00948

o Prevalence 1:500o Mutation of 10 genes coding protein of the cardiac sarcomereo Slight male predominance up to mid-life; female predominance over 60 years of

ageo 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

Restrictiveo Less common

Common Cardiovascular Problems 8

o 50% due to noninfiltrative (familial, diabetic, others) and infiltrative (amyloidosis, sarcoidosis, others)

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 murmurii) Standing (decreased afterload) = increased murmuriii) Valsalva (decreased preload) = increased murmuriv) 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

Case study #12 (in class) – notes Epidemiology

o Increasing incidence and prevalence ~ 5000,000 new cases/yearo > 75% of new and existing cases in 65 and over age group

Pathogenesiso 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 dysfunctiono Systolic dysfunction; inability of the left ventricle to pump blood to the body

Ejection fraction less than 40%

Common Cardiovascular Problems 9

Myocardial contractility Heart rate (↓ SV → ↑ HR → ↓ CO = HF) 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

Signso LVF – S3, raleso RVF – S4, JVD, peripheral edema, hepatomegaly, aciteso In many cases no specific signs

Differential Diagnosiso 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-rayo Brain natriuretic peptide (BNP) – specific to ventricular stretch and correlated with

severityo Echocardiogram

Treatmento Acute

IV loop diuretics and vasodilatorso 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/homeo Requires IV drug therapy, oxygen

Follow-up and preventiono Proper medication useo Guided exercise o Smoking cessationo Weight reductiono Immunization; flu and pneumonia

Common Cardiovascular Problems 10

Common Peripheral Vascular disorders

Occlusive or inflammatory disease in the peripheral arteries, veins or lymphatics.

Differentiation of Arterial and Venous Insufficiency

Sign Arterial Insufficiency Venous InsufficiencyPulse Decreased/absent NormalEdema Absent or mild SignificantPain Severe Absent/mildTemperature Cool NormalColor Pallor with elevation; dusky red on

dependencyHyperpigmentation; cyanotic on dependency

Skin Thin, atrophic; risk of gangrene Thick; risk of stasis ulcerGoolsby, 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

Epidemiologyo Symptoms of lower extremity arterial insufficiency are common in old age.o Affects 12-20% of people older than age 65o Affects 8-12 million individuals of all ages in the United Stateso Age 65-74: Highest rate of newly sx. LEAD– Lower Extremity Arterial Diseaseo In middle age, affects men 2X > womeno Gender disparity begins to disappear after age 65

Pathogenesiso Refers to any occlusive process that limits blood flow to limbs or to vital organs other

than the hearto Underlying atherosclerosis

o Most often due to enlarging atherosclerotic plaques in the distal aorta and its brancheso 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&So 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

Common Cardiovascular Problems 11

o Aortoiliac disease – pain in buttocks or thigh muscleo 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 diseaseo Man or woman age 65-75 who c/o calf aching or burningo Diabetic patient of either sex, with years of suboptimal control

Differential Diagnosiso Venous insufficiencyo Peripheral neuropathyo DJD of lumbar spine

Physical Examinationo General; hair distribution, nails, muscle bulko CVo Lower extremity vascular exam

o Diminished or absent pulseso Blanching with limb elevationo Dependent ruboro Decreased distal skin temperatureo Ulcer’s (tissue loss)

o Lower extremity neurological examo DTRso Sensationo Strength

Diagnostic testingo ABI (Ankle-Brachial Index)

o Normal 1.00 or highero < 0.5 = impaired flow → vascular consult

Treatmento Daily exerciseo Foot careo Treat hypercholesterolemia, HTN and DMo No smokingo Debridement of ulcerso Antiplatelet therapy (aspirin, clopidogrel)o Pentoxifyline or cilostazol, is selected caseso Arterial reconstructive surgery o Percutaneous transluminal angioplasty or stent

Raynaud’s phenomenon

Usually benign, may have underlying disorder (see Faci page 740) S&S

o Fingers blanch, next cyanotic, then red with cold exposure

Common Cardiovascular Problems 12

Treatmento Keep hands warmo CCB or α-adrenergic antagonists, may be helpful

Case study # 13 (in class) – notes

Venous Disease

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)

Essentials Featureso History of prior DVT or leg injuryo Edema, stasis (brawny) skin pigmentation, subcutaneous liposclerosis in the lower lego Large ulcerations at or above the ankle are common (stasis ulcers)

Epidemiologyo One quarter to a third of all adults in western world have varicose veinso 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 systemo 100,000 disabled

Pathogenesiso 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 valveso Potentially life-threatening complication → thrombophlebitis leading to pulmonary

embolio Frequently caused by varicose veins o Often secondary to DVTo Other causes; trauma, pelvic neoplasm, immobilization, pregnancy

S&So Gradual onset of aching, heaviness, tiredness, cramps, itching, burning, restlessness or

pain in lower leg for hours to dayso Question about prolonged immobility or travel

Common Cardiovascular Problems 13

o See the following website for pictures of common findings: http://www.veinclinics.com/cme/skin-findings.html

Differential Diagnosiso DVTo PADo Peripheral neuropathyo 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 Failureo Chronic Renal Failure

Physical Examinationo Pulseso Ankle edema - earliest sign

Check groin to ankle

Common Cardiovascular Problems 14

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 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 stasiso Ulcerso 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 caseso 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-patient-Involvement-Mgt-Lymphovenous.html

o Review website for pictures of ulcers at http://www.bmj.com/cgi/content/full/320/7249/1589

Diagnostic testingo Duplex Doppler ultrasound – accurate for clots in large vessels not small thrombi

Not needed with intact skin and normal pulseso Venography – most accurateo MRI – if ulcer and considering osteomyelitiso Labs to rule out autoimmune/blood disorders

Treatmento Prompt treatment for DVT with anticoagulants ↓ risko Elevation of legs intermittently during the day and at nighto Avoidance of prolonged sitting or standing

Common Cardiovascular Problems 15

o Support or compression stockings (TEDs not enough pressure) If ulcer present use the Rule of 6, see below

Compression Strength Indications8-15mm Leg fatigue, mild swelling, stylish15-20mm Mild aching, swelling, stylish20-30mm Requires prescription-Aching, pain, swelling,

mild varicose veins30-40mm Requires prescription-Aching, pain, swelling,

varicose veins, post-ulcer40-50, 50-60 mm Requires prescription-Recurrent ulceration,

lymphedema

o Unna boot for stasis ulcerso Pentoxifylline may be helpful (consider drug/drug interactions)o Sclerotherapyo Ambulatory phlebectomyo 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

Comparison of 3 common types of leg ulcersVenous Arterial Neuro/DM

Location Garter area of leg-will break down/medial

leg

Pressure sites/toes, heels, foot

Pressure sites/plantar, arches heels, toes

Lesion features Shallow, partial thickness with

irregular borders/shaggy

Punched-out, eschar (blackened if necrotic)

Punched-out

Surrounding skin Hyperpigmented, thickened, with dermatitis-stasis

changes

Hair low, not hyperpigmented,

atrophic

Hair loss, not hyperpigmented,

callus

Palpation findings Non-pitting, tight edema; peripheral

pulses may be normal

Peripheral pulses decreased, capillary refill time increased

Altered sensation with touch, vibration, peripheral pulses

decreased