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Pericarditis: acute

Most common pericardial disease; <6wks, fibrinous, serous; painful

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Pericarditis: subacute

6wks - 6 months; effusive, constrictive

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Pericardidtis: chronic

>6wks; adhesive, effusive, constrictive

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Pericarditis etiologies

Infectious, non-infectious, hypersensitivity/autoimmunity

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Infectious pericarditis: viral

Coxsackievirus A&B, echovirus, mumps, adenovirus, HIV, hepatitis, Epstein-barr

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Infectious pericarditis: bacterial

Pneumococcus, strep, staph, Neisseria, Legionella, Tuberculosis

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Infectious pericarditis: fungal

Histoplasmosis, blastomycosis, coccidiodomycosis, candida, assorted mushrooms

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Other infectious pericarditis

Syphilis, protozoans, parasites

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Non-infectious pericarditis

Trauma, post-irradiation, acute MI (**Dressler’s syndrome), uremia (crystals), primary tumors, metastatic tumors, myxedema (rare dt hypothyroidism); aortic dissection

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*Acute Pericarditis (idiopathic, viral, T-U-M-O-R)

T (tumor, trauma), U (uremia), M (myocardial infarction - **Dressler’s), O (other infxns: bacterial, fungal, TB), R (RA, autoimmune disorders, scleroderma, polyarteritis nodosa, lupus, Radiation)

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Hypersensitivity/Autoimmune causes of Pericarditis

Rheumatic fever; collagen vascular diseases (SLE, RA, scleroderma, Wegener’s granuloma); drug-induced (hydralazine, phenytoin, procainamide, isoniazid, minoxidil, anticoagulants); Postcardiac injury (Dressler’s syndrome, postpericardiotomy, posttraumatic)

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Pericardial Diseases:

Acute pericarditis, pericardial effusion (dt acute pericarditis; inc pericardial fluid), cardiac tamponade (obstruction produced by effusion), constrictive pericarditis (dt chronic pericarditis; rare; scar tissue in pericardial space)

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*Presentation of Acute Pericarditis

sudden onset severe chest pain waxes/wanes w/movement (*worse lying supine; better sitting up and leaning forward); worse w/deep breathing/cough; pain radiates along ligamentous attachments (retrosternal, neck, L shoulder/arm), fever dt inflam/virus

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*Differential for Acute Pericarditis

acute MI or other acute coronary event; pulmonary embolism; aortic dissection; pneumothorax; pneumonia, pericardial effusion/cardiac tamponade

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*Diagnostic key findings for Acute Pericarditis

*pericardial friction rub* (high-pitched, scratching, grating heart sounds when pt is sitting;* ECG is most IMPORTANT tool (widespread concave ST elevations at 2-3 limb leads & V2-V6; serology inconclusive (usu elev WBC/ESR)

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Chronic Relapsing acute Pericarditis

~25% of acute idiopathic cases; at risk for constrictive pericarditis; longer prednisone taper? Consider pericardiectomy

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Bacterial Pericarditis

Rare; intrathoracic spread of pneumonia/empyema/endocarditis; usu missed b/c lack of typical findings…usu fatal

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Acute Pericarditis Dx & Tx

viral/idiopathic if CP worsens w/motion; cardiac rub on auscultation; characteristic ECG; neg cardiac enzymes, no evidence of TUMOR, HIV, effusion, tamponade; negative echo; expect full recovery in 1-4wks w/bedrest & anti-inflamm; rule out TB w/skin test

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Tuberculosis Pericarditis

<8% of pulmonary cases; presents w/typical TB signs (night sweats, wt loss); Dx w/sputum or bronchoscopy + pericardial biopsy

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Uremic Pericarditis

Usu in pts w/uremia from end-stage renal Dx who are undergoing chronic hemodialysis

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**Post-AMI Pericarditis (Dressler’s Syndrome)

<15% of AMI pts develop w/in 3 months; cause not clear; presents w/fever, sharp pain, friction rub; rely on Hx, ECG, labs to rule out new AMI; Tx bedrest, ASA, NSAIDs

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Chronic Constrictive Pericarditis

Confused w/restrictive cardiomyopathy dt similar presentation w/JVD Kussmaul’s sign that inc w/inspiration; sustained venous pressure (peripheral edema, hepatomegaly, ascites)

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How to differentiate constrictive pericarditis from chronic constrictive pericarditis

Hearing a diastolic (pericardial) knock 3rd heart sound, but no other murmurs

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Pericardiocentesis

Subxiphoid puncture to avoid major epicardial vessels; guidewire, flexible catheter drains fluid

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Chronic Constrictive Pericarditis

Formation of scar tissue in pericardial cavity following healing of acute or chronic relapsing pericarditis; can be calcified, idiopathic, cardiac surgery, TB, radiation, autoimmune disorders

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Chronic constrictive pericarditis lab visualization

MRI or CT scans are most sensitive/specific for thickening; CXR can show pericardial calcification

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Chronic constrictive pericarditis treatment

Pericardial resection (pericardectomy or cardiac decortication); full improvement can take months

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Acute pericarditis summary

Positional pain, friction rub, widespread ST elevations, treat w/anti-inflammatories

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Pericardial effusion summary

Part of the continuum btw pericarditis and tamponade; may require pericardiocentesis

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Cardiac tamponade summary

Increased venous pressure, pulsus paradoxus, diagnostic echocardiogram, treat w/pericardiocentesis

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Constrictive pericarditis

Signs of right heart failure, diastolic knock, Kussmaul’s sign, diagnostic CT or MRI, treat w/pericardiectomy

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Acute Endocarditis

Most common endocarditis, febrile, erratic spiking fevers, rapid damage to heart, seeds extracardiac sites via blood, progresses to death w/in wks, usu a/w IVDA; 10/100,000 per yr

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Subacute Endocarditis

Indolent course, rarely febrile, rarely damaging, rarely spread by blood; gradual progression; rarely causes death unless a/w major embolism/ruptured mycotic aneurysm

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Populations at risk for endocarditis

Abnormal/damaged heart valves, prosthetic valves, intravascular appliances (ex: indwelling catheters, elderly, IVDA

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4 Bugs a/w endocarditis

Streptococcus (native valve & long-term prosthetic valves); Pneumococci (community acquired native valves); Enterococci (nosocomial native & prosthetic valves); Staphylococci (IVDA

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Other bugs a/w endocarditis

Gram-negative bacilli; HACEK group (fastidious G-neg coccobacilli); Candids; polymicrobial

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Clinical Features of Endocarditis

Fever, chills, sweats, anorexia, wt loss, new heart murmur, worsening murmur, arterial emboli, splenomegaly, petechiae

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Peripheral manifestations of endocarditis: Janeway Lesion

Flat, painless bluish/purplish lesion on palms or soles; CLASSIC dt bacterial embolis spit out by heart valve and gets stuck in skin

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Peripheral manifestations of endocarditis: Roth Spots

Small erythematous rings dt bacterial emboli from infected valve

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Peripheral manifestations of endocarditis: others

Petechiae and splinter hemorrhages on nails

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Peripheral manifestations of endocarditis: Osler’s Nodes

Painful, red, raised nodules (differentiate from Janeway lesion); usu on sides of fingers/toes or thenar/hypothenar eminences

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Clinical Criteria for Dx of Infective Endocarditis (IE): Major

1. Positive blood culture for typical microbe from 2 separate draws OR persistently positive cultures; 2. evidence of endocardial involvement (pos echo w/oscillating intracardiac mass/abscess/partial detachment of prosthetic valve, new valve regurgitation

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Clinical Criteria for Dx of Infective Endocarditis: Minor

1. predisposing heart dx or IVDA; 2. Fever >100.4F; 3. Vascular phenomena; 4. Microbiologic evidence not meeting major criterion; 5. Consistent echo results not meeting major criterion

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Common treatment regimens: Penicillin-sensitive Strep bovis or Strep viridans

Penicillin G, IV q6h for 4wks OR Penicillin G q6h + Gentamycin q8h for 2wks OR Ceftriaxone IV or IM 1qd for 4wks

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Common treatment regimens: Relatively penicillin-resistant S. bovis or viridans

Penicillin G + Gentamyxin OR Vancomycin

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Methicillin-sensitive staphylococci w/o prosthesis

Nafcillin + Gentamycin OR 1st generation cephalosporin

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Methicillin-resistant staphylococci w/o prosthesis

Vancomycin

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Methicillin-sensitive staphylococci in uncomplicated tricuspid endocarditis

Nafcillin + Gentamycin

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Methicillin-resistant staphylococci w/prosthesis

Vancomycin + Gentamycin OR Vancomycin + Rifampin

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Myocarditis

Any inflammation or degeneration of the heart; usu diagnosed from autopsy! Endomycardial biopsy may provide greater insight into pathogenesis/etiology/treatment

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Important causes of myocarditis

Infection (viral, bacterial, rickettsial, spirochetal, protozoan, metazoan, fungal); Toxic (anthracyclines, catecholamines, IL-2, IFN-a2); Hypersensitivity

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Myocarditis: Viral infections

Cocksackie A&B, echo, influenza A&B, polio, herpes simplex, varicella zoster, Epstein-barr, cytomegalovirus, mumps, rubella, rubeola, vaccinia, coronavirus, rabies, hepatitis B, arbovirus, junin virus, HIV

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Myocarditis: Bacterial

C. diptheriae, Salmonella typhi, b-hemolytic strep, N. meningitides, legionella pneumonophilia, listeria monocytogenes, campylobacter jejuni, coxiella burnetti (Q fever), Chlamydia trachomatis, mycoplasma pneumoniae, chlamydia psittaci, M. tuberculosis

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Myocarditis: Rickettsial, Spirochetal, Protozoan, Metazoan

rickettsia rickettsii (rocky mountain), borrelia burdorferi (lyme); Trypanosoma cruzi (Chagas); Toxoplasma gondii; Trichinosis, Echinococcosis

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Myocarditis: Fungal

Aspergillosis, blastomycosis, candidiasis, coccidioidomycosis, cryptococcosis, histoplasmosis, mucormycosis

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Myocarditis: Drug-induced hypersensitivity

Antibiotics, anticonvulsants, antituberculars, anti-inflammatories, diuretics, others

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Myocarditis: Clinical manifestations

Acute usu asymptomatic; 60% flu-like; 35% HF/CP; mimic acute MI w/ventricular dysfxn, ischemic CP; ECG: injury or Q-waves; syncope, palpitation w/AV block or ventricular arrhythmia; sudden death; systemic//pulmonary thromboembolic disease

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Myocarditis: Blood studies

ESR: 60%; WBC elevation 25%; CK-MB elevation 12%; a 4-fold rise in IgG titer over 4-6wk period is required to document acute viral infxn; heart specific Ab are non-specific for myocarditis (also found in dilated cardiomyopathy)

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Myocarditis: Echocardiography

Useful in managing pts w/acute myocarditis; LV systolic dysfxn common w/abnml segmental wall motion; LV size is usu nml; slight wall thickness; 15% ventricular thrombi

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Myocarditis: Imaging studies

Gallium 67 for inflammation; Indium 111-antimyosin monoclonal antibody for injured myocardium

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Myocarditis: diagnostic standard

Endomycardial biopsy!

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Myocarditis: Treatment

Usu self-limited; manage LV dysfxn like other CHF/AV blocks; *caution: exercise may intensify inflammation; consider anticoagulant to prevent thromboemboli; temporary pacer for complete AV block

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Cardiomyopathy

Primary disorder of heart muscle; not caused by inflammation; it manifests as CHF; classified by pathophysiology and clinical presentation

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Dilated 1* Cardiomyopathy

Congestive/DCM; ventricular enlargement and systolic dysfxn; may look like pericardial effusion on CXR

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Hypertrophic 1* Cardiomyopathy

HCM; inappropriate myocardial hypertrophy in absence of hypertension or aortic stenosis

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Restrictive 1* Cardiomyopathy

Infiltrative; abnormal filling and diastolic function

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Secondary Cardiomyopathies - specific heart muscle disease

Infectious, metabolic, systemic disease, familial, sensitivity, toxic

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Idiopathic Dilated Cardiomyopathy

Dx of unknown etiology affecting myocardium w/LV dilation, hypertrophy, and fibrosis; <10/100,000/yr; middle aged; death dt progressive pump failure; 30% 5yr survival; dx may stabilize but rarely recover completely

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Idiopathic Dilated Cardiomyopathy: Pathophysiology

Dec systolic fxn results in dec cardiac output; in advanced disease fibrosis develops, most pts deteriorate progressively despite treatment; dt combo of genetic, environmental, immunologic factors

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Idiopathic Dilated Cardiomyopathy (IDC) Hx and Physical Findings

Sx of heart failure (dyspnea, orthopnea w/ Left HF); Peripheral edema (Right HF); fatigue and weakness (low CO); hypotension, tachycardia, tachypnea, JVD, 3rd/4th heart sounds?; tricuspid or mitral murmurs/regurgitation

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DCM Cardiac Imaging

CXR (enlarged cardiac silhouette); ECG (LVH, BBB); echocardiogram, holter monitor, radionucleotide vetriculography

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IDC Management

Treat CHF (salt restriction, diuretics, digitalis, antihypertensives); anticoagulants (dec risk of thromboembolism), pacemaker/cardioverter-defribrillator; cardiac transplant

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Causes of DCM

Myocarditis (#1 is coxsackievirus B; staph, enterococci); HIV, Chagas disease (T. cruzi); Lyme carditis; Alcohol (#2 most common 2* cause); prepartum cardiomyopathy (30% mortality); drug-induced (cocain, antineoplastic agents); muscular dystrophies

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Hypertrophic Cardiomyopathy

LV hypertrophy; histopath = disorganized myocardial cells; results in dec LV cavity/stiffness; impaired diastolic filling, inc filling pressure; outflow obstruction w/septal hypertrophy (produces systolic anterior motion of mitral valve leaflet)

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Characteristics of Hypertrophic Cardiomyopathy (HCM)

Aka: …subaortic stenosis OR hypertrophic obstructive cardiomyopathy; affects 0.2% of pop; 50% hereditary/idiopathic; variable prognosis; sudden death <30yo, Hx of syncope, family Hx of sudden death; <15% develop DCM

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HCM Pathophysiology

Systolic (outflow tract gradiant); Diastole (impaired diastolic filling; inc pressure); Myocardial ischemia (inc muscle mass, filling pressure, O2 demand; dec vasodil capacity, dec capillary density; abnml intramural coronary aa; systolic aa compression)

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Asymmetric Septal Hypertrophy w/Obstruction

Blood leaks back thru mitral valve = mitral regurgitation; mitral valve presses against septum causing obstruction to blood flow thru aortic valve; systolic anterior motion of mitral valve (SAM)

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3 mechanisms causing intensification of dynamic pressure gradient in HCM

inc L ventricular contractiliy; dec ventricular volume (preload); dec aortic impedance and pressure (afterload)

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Increase in gradient and loudness of murmur in HCM

Produced when contractility increases w/exercise or by reducing ventricular volume w/a valsalva, sudden standing or nitroglycerin

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Decreased pressure gradient and loudness of murmur in HCM

Elevating arterial pressure w/squatting or sustained handgrip; increasing venous return w/passive leg raising or expanding blood volume

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HCM Cardiac Imaging - best test

**2D echocardiogram** LVH, small left ventricular cavity, thickened septum

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Clinical manifestation of HCM

**Hallmark - harsh systolic murmur that begins after 1st heart sound best heard at L sternal border and apex**Asymptomatic (found on echo after hearing murmur); Symptomatic (dyspnea, angina pectoris, fatigue, pre-syncope, syncope inc risk of SCD in youth;

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Recommendations for patients <30yo if HCM is proven

Avoid competitive sport/dehydration; b-adrenergic blockers dec angina and syncope in 50%; Amiodarone dec risk of arrhythmias; maintain sinus rhythm w/pace maker; implant defribrillator?; myotomy if septum is severe; screen all 1st degree relatives for HCM

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Recommendations for patients >30yo if HCM is proven

Low-risk pts sports ok: no V-tach on Holter, fam Hx of sudden death dt HCM, Hx of syncope/impaired consciousness, severe hemodynamic probs, exercise induced hypotension, mitral regurgitation, enlarted L atrium, paroxysmal atrial fib, abnml heart perfusion

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Restrictive Cardiomyopathy

*hallmark: abnormal diastolic function;* rigid ventricular wall w/impaired filling (stiff heart w/o enlargement); similar to constrictive pericarditis; prognosis is poor b/c cause is progressive

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RCM Etiology

Dt development of endomycardial fibrosis that stiffens ventricle; dt eosinophilia (Loeffler’s syndrome), amyloidosis, hemochromatosis, rxn to chemo/radiation or scleroderma, sarcoidosis, metastatic malignancy

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RCM Pathophisiology

Cavity of LV is normal size, but stiff; short filling time; limited CO and inc filling pressure (causes dyspnea and exercise intolerance); persistently elevated venous pressure (edema, ascites, large liver); pts present w/RHF or LHF

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RCM Cardiac Imaging

CT or MRI (identifies constrictive pericarditis); Endomyocardial biopsy (will identify myocardial fibrosis, amyloidosis, hemochromatosis, and other disorders)

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RCM Treatment

No good therapy; drug therapy used w/caution (diuretics for high filling pressures, vasodilators may dec filling pressure, ?Ca-channel blockers to improve diastolic compliance, digitalis/inotropic NOT indicated)

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Pts at risk of STEMI (ST-Elevation Myocardial Infarct)

all pts should have risk factors identified every 3-5yrs;

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Recommended Cholesterol levels; what drugs lower cholesterol, what are the side effects?

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Opportunities for Dr. intervention prior to occlusive coronary MI

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Patients taking nitroglycerine for angina should only take one pill; if pain doesn't improve in 5 min...

call 911 immediately; pts may receive instructions to chew aspirin (165-325mg) if not contraindicated or may receive aspirin en route to hospital

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Physical exam for pts being evaluated for MI

ABCs, vital signs, general observation, JVD?, pulmonary auscultation (rales), cardiac auscultation (murmurs/gallops), stroke?, pulses?, systemic hypoperfusion (cool, clammy, pale, ashen?)

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Differential Diagnosis of STEMI: life threatening

aortic dissection, pulmonary embolus, perforating ulcer, tension pneumothorax, boerhaave syndrome (esophagus rupture w/mediastinitis)

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Differential Diagnosis for STEMI: other CV and non-ischemic problems

pericarditis, atypical angina, early repolarization, Wolff-Parkinson-White syndrome, deeply inverted Twaves (CNS lesion/apical hypertrophic cardiomyopathy), LV hypertropy, Brugada syndrome, myocarditis, hyperkalemia, BBB, vasospastic angina, HCM

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Differential Diagnosis of STEMI: other non-cardiac problems

gastroesophageal reflux (GERD) and spasm, chest-wall pain, pleurisy, peptic ulcer disease, panic attack, cervical disc or neuropathic pain, biliary/pancreatic pain, somatization and psychogenic pain disorder

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Aspirin is the 1st drug administered to pt suspected of MI

dose up to 325gm; containdications are: allergy, active peptic ulcer, recent Hx of GI or intracranial bleed, haemophilia, von Willebrand's disease, thrombocytopenia, severe liver disease

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Prehospital issues related to STEMI

defibrillator capable; prehospital fibrinolysis (EMS to needle w/in 30min); EMS transport (EMS to balloon w/in 90min)

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PCI (percutaneous coronary intervention)

the best anti-thrombosis therapy; alternative is use of lytic agents like TPA

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Contraindications of TPA use

intracranial bleed, cerebrovascular lesion/tumors, ischemic stroke, suspected aortic dissection, active bleeding (incl menses), significant closed-head/facial trauma; others: anticoagulants, prior stroke, glucose levels, hi BP, seizure, pregnancy

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If EKG shows inferior infarct, obtain R side leads for:

screen for R ventricular infarct, a common complication of inferior MI

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Cardiac enzyme markers that are highly diagnostic for MI and more reliable than ECG:

Cardiac troponins and MB isozyme of CK; they can rule out MI in pts w/confusiong ECG or LBBB

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Other drugs used emergently for STEMI

O2, nitroglycerin, morphine, b-blockers

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PCI vs Fibrinolysis for STEMI: which has best outcome?

PCI if w/in time limits ~60min; an antithrombolytic may need to be administered if there is a delay in getting to the PCI

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Other drugs used emergently for STEMI:

O2, Nitroglycerine (unless systolic BP <100mmHg, HR <50bpm, suspected RV infarct, use of phosphodiesterase inhibitor for erectile dysfxn in last 24hrs); Morphine (pain management); b-blockers (universally good)

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STEMI Imaging:

CXR (rule out other pathology incl aortic dissection); TTE or TEE; contrast chest CT or MRI

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Lytic therapy: most commonly used

TPA and Emminase

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Use of TPA and the relationship with the ECG:

DON'T give to pt w/STdepression! Give to STEMI pts w/symptom onset w/in 12hrs &12-lead ECG a/w true post MI; Also give to pts w/STEMI symptoms for 12-24hrs w/continued ST elevation >0.1 and >2 precordial or limb leads

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Findings a/w reperfusion assessment:

relief of symptoms, maintenance and restoration of hemodynamic and/or electrical instability; reduction of >50% of initial ST-segment elevation pattern on follow-up ECG 60-90min after initiation of therapy

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Use of Heparin therapy

given to pts undergoing PCI or surgical revascularization; after alteplase, reteplase, tencteplace; after streptokinase, anistreplase, urokinase in pts at hi risk for systemic emboli; Vit K can REVERSE effect

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Clopidogrel (plavix) indications:

for pts receiving fibrinolytic therapy who are unable to take aspirin b/c of hypersensitivity or GI intolerance; used after stent placement, MI, and has use w/angina; it is a cardio preventive drug

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ACE and ARBs (angiotensin receptor blockers)

inhibit renin-angiotensin-aldosterone system; given orally w/in 24hrs of STEMI to pts WITHOUT hypotension, anterior MI, previous MI, CHF/pulmonary congestion, LVEF <.4

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Right Ventricular Infarction: ECG findings

ST elevation in R sided leads

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Right Ventricular Infarction: Clinical findings, hemodynamics, echo, Rx

shock w/clear lungs, elevated JVP, Kussmaul sign w/breath; Inc RA pressure; Depressed RV function; Maintain RV preload, lower RV afterload, inotropic support, reperfusion

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VPB arrhythmia: Treatment

"electrical instability;" K+, Mg++, b-blocker

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VT arrhythmia: Treatment

"electrical instability;" antiarrhythmics, DC shock

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AIVR arrhythmia: Treatment

"electrical instability;" bserve unless hemodynamic compromise

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NPJT arrhythmia: Treatment

"electrical instability;" search for cause; ex: digoxin toxicity

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Sinus tachycardia: Treatment

"pump failure/excess sympathetic tone;" treat cause; b-blocker

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Atrial fibrillation/flutter: Treatment

"pump failure/excess sympathetic tone;" treat cause; slow ventricular rate; DC shock

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PSVT: Treatment

"pump failure/excess sympathetic tone;" vagal maneuvers, b-blocker, verapimil/diliazen; DC shock

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Sinus bradycardia: Treatment

"bradyarrhythmia;" treat if hemodynamically unstable; atropine/pacing

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Junctional arrhythmia: Treatment

"bradyarrhythmia;" treat if hemodynamically unstable; atropine/pacing

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Smoking and STEMI

encourage pt and family to stop; provide counseling, pharm therapy, formal smoking cessation programs

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Lowering BP and STEMI

>120/80: control wt, exercise, moderate EtOH, restrict Na, healthy diet; *if >140/90, chronic kidney dx or diabetes: add b-blockers, inhibitors of renin-angiotensin-aldosterone system and drop down to <130/80

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Exercise and STEMI

encourage 30-60 min of activity, at least 3-4x/wk

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Lipid management and STEMI: TG < 200mg/dL

Goal: get LDL-C << 100mg/dL; use statins; start healthy diet w/<7% calories from sat fat and <200mg/d cholestrol; inc activity; wt managment; omega-3 FAs)

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Lipid management and STEMI: TG > 200mg/dL

Goal: get non-HDL-C << 130mg/dL; wt managment, inc activity, stop smoking; add fibrate or niacin; consider omega-3 FAs as adjunct for high TGs

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Weight management and STEMI

goal: BMI 18.5-24.9kg/m^2; waist circumference <35 for women, <40 for men

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Diabetes management and STEMI

goal: HbAlc < 7% near normal fasting plasma glucose; inc activity, manage wt, manage BP and cholesterol too

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Post-MI: ACE inhibitors

(renin-angiotensin-aldosterone system blockers); use in all pts indefinately

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Post-MI: b-blockers

use indefinately in all pts

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Post-MI: Aspirin

administer 75-162mg/day (or 75mg/d clopidrogel or INR 2.5-3.5 warfarin)

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Plaque formation marker

cholesterol LDL

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Inflammation markers (many factors, infxn?)

C-reactive protein, adhesion molecules, IL-6, TNF-a, aCD-40 ligand

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Plaque rupture markers (MQs, MMPs)

MDA modified LDL

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Thrombosis markers (platelet activation, thrombin)

D-dimer, complement, fibrinogen, troponin, CRP, CD40L

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Acute coronary syndrome (ACS) clinical spectrum includes:

Non-ST-segment elevation [including: unstable angina (UA), non-Q-wave myocardial infarction (NQMI)], and ST-segment elevation MI (STEMI)

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Coronary thrombosis results from

a rupture of an unstable plaque with resultant thrombus formation

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Unstable plaques are characterized by:

a large lipid-rich core and only a thin, fibrous cap, which is vulnerable to rupture or erosion by inflammatory cells and activated macrophages

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The leading cause of death worldwide:

Atherothrombosis

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Correlation of 6-month mortality w/baseline ECG findings in pts w/ACS

risk of 6-month mortality is as great as pts w/STEMI; emphasize the improtance of aggressive in-hospital and post-discharge therapy!

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Braunwald Classification of High Risk Pts w/Unstable Angina

elevated TnT cardiac marker; ECG (angina at rest w/transient ST-seg changes, new BBB, sustained V-tach); PE (pulmonary edema, new/worse MR murmur, S3 or new/worse rale, hypotension, bradycardia, tachycardia, >75yo)

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Braunwald Classification of Moderate Risk Pts w/Unstable Angina

slightly elevated TNT cardiac marker; ECG (T-wave inversion, pathological Q-waves); >70yo

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Braunwald Classification of Low Risk Pts w/Unstable Angina

normal cardiac markers; ECG (normal/unchanged ECG during episode of chest discomfort)

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ACS marker: Troponin

the greater the levels in pts presenting w/NSTE-ACS, the greater the risk of future mortality (actually, even small amounts are a/w risk of inc mortality)

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ACS marker: B-type naturitic peptide (BNP)

a/w relative mortality risk

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Management of Cardio-ischemia

bed rest, continuous ECG monitoring, supplemental O2 for SaO2 >90%; NTG, b-blockers, IV morphine, IABP for hemodynamic instability, ACEI for persistent hypertension in pts w/LV systolic dysfxn or CHF

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Anti-platelet therapy

to prevent platelets from adhering to plaque fissure or rupture; activation/aggregation leading to thrombotic occlusion; reduces risk of MI

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Aspirin and platelets

blocks activation of platelets by arachidonic acid

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Thienopyridines (ticlopidine and clopidogrel) and platelets

block ADP-mediated platelet activation

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Antithrombin therapy (heparin, low MW-heparin, direct thrombin inhibitors) and platelets

blocks thrombin-mediated platelet activation

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Glycoprotein IIb/IIIa inhibitors and platelets

block platelet aggregation by inhibiting fibrin from binding to GPIIb/IIIa receptor

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Contraindications of GPIIb/IIIa Therapy

active or recent bleeding; severe hypertension, any intracranial bleeds/lesions/tumors; major surgery/trauma, thrombocytopenia (<100,000); bleeding diathesis/warfarin w/elevated INR; avoid w/renal insufficiency/failure

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Two types of Heparin:

Low MW Heparin (enoxaparin; SQ); Unfractionated Heparin (UFH; IV)...Enoxaparin is perferred unless CABG is planned w/in 24hrs

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Heart Failure

clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill w/ or eject blood (dyspnea/SOB, fatigue, peripheral edema, JVD, BBB)

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Congestive Heart Failure Stats

5 million pts; 6.5 million hospital days/yr; 300,000 deaths/yr; 6-10% of people >65yo; 5.4% of health care budget ($38 billion); Incidence has doubled in last 10yrs

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BNP (brain naturetic peptide)

direct correlation btw concentration and end diastolic pressure in left heart; can reflect heart failure

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Echocardiogram

the single best diagnostic imaging tool for heart failure (also cost effective)

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Suspected heart failure dt Signs/Sx:

assess presence of cardiac disease by ECG, CXR, BNP; If tests are abnormal do a ventricular fxn test by ECHO-doppler; If abnormal, pt has heart failure (systolic/diastolic); Identify etiology, evaluate severity, choose therapy

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Stages in the evolution of heart failure

1. HF risk w/o disease or symptoms; 2. Heart disease w/o symptoms; 3. Asymptomatic LV dysfunction; 4. Prior or current HF symptoms; 5. Refractory HF symptoms

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Stages in the evolution of heart failure: Clinical Characteristics

1. Hypertension, diabetes, elev cholesterol, fam Hx, cardiotoxins; 2. Heart disease (any); 3. Asymptomatic LV dysfxn; 4. Dyspnea, fatigue, dec exercise tolerance; 5. Marked symptoms at rest despite max therapy

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Stages in the evolution of heart failure: Treatment

1. Treat risk factors, avoid toxics, ACE-i in selected pts; 2/3. ACE-i, b-blockers in selected pts; 4. ACE-i, b-blockers, diuretics, digitalis; 5. Palliative therapy, mechanical assistive device, heart transplant

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Major risk factors for CHF

coronary heart disease, high bp, CRP >7mg/L, ankle-arm index <0.9, inter-carotid wall thickness >1.88mm, diabetes

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Direct causes of CHF

myocardial abnormalities (CHD), Hemodynamic overload, ventricular filling abnormalities, ventricular dyssynergy (abnml rhythm: ie LBBB where septum and lat wall contract), changes in cardiac rhythm

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Major aggravating factors in CHF

medications (ex: Celebrex/Vioxx), new heart disease, myocardial ischemia

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Initial/Ongoing Evaluation of CHF patients

identify heart disease, assess LVEF and fxnl capacity, assess volume status (use of diuretics: edema, rales, JVD, hepatomegaly, wt), lab assessment (electrolytes, renal fxn, repeat ECHO), assess prognosis

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Prognosis is exponentially related to the LVEF

if LVEF is >40%, the prognosis is fairly good (90%)

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Treatment objectives

inc survival, exercise capacity, quality of life, AND decrease morbidity, neurohormonal changes, progression of CHF, symptoms, cost

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Treatment strategies

prevention (control risk factors), change lifestyle, treat etiologic cause/aggravating factors, drug therapy, personal care (team work)

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Treatment strategies for selected patients

revascularization if ischemia causes HF, ICD (implantable cardiac defibrillator), ventricular resynch, ventricular assist device, transplant, artificial heart, neoangiogenesis, gene therapy

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CHF Treatment: Pharmacologic Therapy

diuretics, ACE-i, b-blockers; (also: digitalis, spironolactone - improves survival)

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Diuretics

essential to control symptoms secondary to fluid retention (edema, dyspnea, lung rales, JVD, hepatomegaly, pulmonary edema); prevents progression from HT to HF

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Thiazide diuretics

inhibit the active transport of Cl-Na in the cortical diluting segment of the ascending limb of the loop of Henle

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Loop diuretics

inhibit the transportof Cl-Na-K in the think portion of the ascending limb of the loop of Henle

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Potassium-sparing diuretics

inhibit the reabsorption of Na in the distal convoluted and collecting tubules

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ACE-Inhibitors

block conversion of angiotensin I to angiotensin II; blocks vasoconstriction, aldosterone, vasopressin, and sympathetics; Increase kinin levels (potent E2, F2 vasodilators) and inc release of fibrinolytic substances like tPA

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ACE-Inhibitors: Adverse Effects

Hypotension (1st dose effect); worsening renal fxn, hypokalemia, cough, angioedema, rash, ageusia, neutropenia

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ACE-Inhibitors: contraindications

intolerance (angioedema, anuric renal failure), bilateral renal artery stenosis

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Beta-blockers: benefits from MOA

increase density of B1 receptors; inhibit cardiotoxicity of catecholamines, decrease neurohormonal activation, decrease HR, anti-ischemic, anti-hypertensive, anti-arrhythmic, anti-oxidant, anti-proliferative

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Beta-blockers: Contraindications

*asthma (reactive airway disease); AV block (unless pacemaker), symptomatic hypotension/bradycardia

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Digitalis (digoxin):MOA

inhibits Na-K ATPase pump; increases intracellular Na; activates exchange of Na and Ca; increased influx of Ca ==> increased cardiac contractility

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Digitalis: contraintications

digoxin toxicity

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Spironolactone

competitive antagonist/inhibitor of aldosterone receptor; decreased retention of Na and water (decreases edema), and increased excretion of K+ and Mg2+ (decreases arrhythmias), also decreases collagen deposition (dec fibrosis)

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B-blockers: adverse effects

hypotension, fluid retention/worsening heart failure, fatigue, bradycardia/heart block (discontinue only in severe cases)

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Inotropics

used for selected pts w/refractory HF

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Nitrates

used in selected pts w/ischemia, angina, pulmonary congestion

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ARB

used only in selected pts; contraindications to ACE-i

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Antiarrhythmics

(only amiodarone) used in selected pts w/High risk arrhythmias

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Anticoagulants

used in selected pts w/high risk of embolism

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Ca channel blockers

only amlodipine; used in selected pts w/ischemia

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Angiotensin II Receptor Blockers (ARB)

selective/competitive blocks against antiogensin II; prevents binding to the AT1 receptor; prevents vasoconstriction and proliferation; indicated in pts intolerant to ACE-i; ex: losartan, valsartan, irbersartan, candersartan

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Nitrates

have hemodynamic effects: 1. venous dilation (dec preload: dec pulmonary congestion, ventricular size, ventricular wall stress, MVO2); 2. Coronary vasodilation (inc myocardial perfusion); 3. Arterial vasodilation (dec afterload, dec CO, dec BP)

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Nitrates: clinical usage

CHF w/myocardial ischemia, orthopnea and paroxysmal nocturnal dyspnea, acute CHF/pulmonary edema, hypotension, renal insufficiency when intoerant to ACE-i

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Positive inotropes:

Digitalis; Sympathomimetics (catecholamines, b-adrenergic agonists); Phosphodiesterase inhibitors (amrinone, milrinone, enoximone); Calcium sensitizers (levosimendan, pimobendan)

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Positive inotropes: clinical usage for CHF

intended to inc contractility and CO to meet metabolic needs of body; *Refractory CHF a/w dec systolic fxn and cardiomegaly, depression of ejection fraction and elevated LV filling pressure; not for chronic therapy

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Supraventricular arrhythmias

at risk for emboli; treat w/b-blocker, digitalis; second choice amiodarone; (c. Understand that when a person converts to sinus rhythm they are at risk of emboli)

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Ventricular Arrhythmias

antiarrhythmic are ineffective; b-blockers reduce mortality and sudden death; control ischemia; control electrolyte distrubances; ICD (implantable cardiac defibrillator) is secondary prevention of sudden death, in sustained hemodynamic destabilizing VT,

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Know how to differentiate diastolic heart failure from systolic (R vs. L sided)

Right heart failure: JVD, ascites in abdomen vs. lower leg edema; no crackles in lungs but may have significant abnormal lung fxn

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Diastolic heart failure

wrong dx of HF or LVEF; 1* valve dx; restrict/infiltrat cardiomyopathy; pericardial constrict; episodic/reversible LV systol dysfxn; HT, ischemia; anemia/thyrotoxicosis; chronic pulm dx w/RHF; pulm HT; atrial myxoma; LVHypertrophy; diastolic dysfxn

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Diastolic heart failure: treatment

treats as HF w/low LVEF; control hypertension, tachycardia, fluid retention, myocardial ischemia; Nitrates, diuretics

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Heart Failure Models

Congestive (digoxin, diuretics); Hemodynamic (vasodilators); Neurohumoral (ACE inhibitors, b-blockers, spironolactone); Immunological (cytokine inhibitors)

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Treatment strategies for CHF

Symptom relief (diuretics, vasodilators, inotropics); Prevention of dx progression (neurohormonal activation, ACE-i, b-blockers, spironolactone, ARBs?, ANP?, ET-1?); Reversal of HF (gene therapy?, anti-remodeling strategies?)

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Recommendations for evaluation of pts: Class I

1. H&P; 2. ability to perform activities; 3; Volume status (edema/retention); 4. Lab (blood count, electrolytes, creatine, glucose); 5. initial 12-lead ECG, CXR; 6. Initial 2D Echo or ventriculography for LV systolic fxn; 8. coronary arteriograph w/angina

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Recommendations for pts at high risk of developing HF: Class I Stage A

1. control systolic and diastolic HT; 2. Tx lipid disorders; 3. control other risks (smoking, EtOH, drugs); 4. ACE-i for atherosclerotic, DM, HT pts; 6. Control ventricular rate in supraventricular arrhythmias; 6. Tx thyroid; 7. eval signs/Sx of HF

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Recommendations for pts at high risk of developing HF: Class IIa, Stage A

non-invasive evaluation of LV fxn in patients w/strong family Hx of cardiomyopathy or in those receiveing cardiotoxic interventions

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Recommendations for pts w/asymptomatic LV systolic dysfxn: Class I, Stage B

ACE-i in pts w/previous AMI or reduced LVEF; B-blockade in pts w/recent AMI or reduced LVEF; valve repair for valvular stenosis/regurgitation; regular eval for signs/symptoms of HF; also Class I recommendations for stage A pts

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Recommendations for Tx of Symptomatic LV Systolic Dysfxn: Class I, Stage C

diruetics for fluid retention; ACE-i in all pts; b-blockers in all stable pts; digitalis for Sx of HF; Withdrawal of drugs adversely affecting clinical status (usu antiarrhythmics, Ca-blockers, non-steroidal/anti-inflammatory drugs

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Recommendations for Tx of Symptomatic LV systolic dyxfxn: Class IIa, Stage C

Spironolactone, exercise, angiotensin receptor blocker in pts avoiding ACE-i b/c cough or angioedema; hydralazine and a nitrate in pts who can't be given ACE-i b/c of hypotension or renal insufficiency

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Recommendations for pts w/Refractory End-stage HF: Class I, Stage D

meticulous identification/control of fluid retention; referral for cardiac transplantation in eligible; referral to HF program; other class I recommendations for Staget A, B and C!

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Cardiac Myxoma

most common primary cardiac tumor; benign; obstructive cardiac symptoms (pulmonary edema, progressive cardiac failure, embolic symptoms); Constitutional symptoms (dt associated endocrine problems, ex: Carney Complex - acromegaly); presents in 40-50yo

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Most common complication with cardiac myxoma

mitral valve obstruction...no blood into Left ventricle prevents cardiac output

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Cushings disease and myxomas

although related, myxomas are so rare that you may never find a cushing's pt w/one

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Metastatic Cardiac Tumor

most common heart tumors seen; NOT PRIMARY; usu from breast, lung; cardiac tamponade from compression on ventricle and dec cardiac output; pt can die

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Angiosarcoma

malignant tumor; non-specific, possible chest pain, SOB, malaise, fever

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Familial cardiac myxomas

occurs w/other abnormalities as "Carney Complex." Musculoskeletal manifestations; perinatal myosin heavy chain is underlying cause of Carney complex variant (**mutation of contractile proteins relevant to cardiac tumorigenesis)

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Why is heart disease bad?

it's worse than cancer b/c 50% of diagnosed will be dead in 2years if you can't fix the problem; most are valvular abnormalities

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Congenital Valvular Disease

bicuspid aortic valve is most commonly seen in adult cardiology

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Acquired valvular disease

Degenerative, rheumatic, inflammation, infectious (endocarditis), functional (mitral/tricuspid valves)

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Prosthetic valvular disease

Any prosthesis put into a heart is considered abnormal…make sure it is better than what is being replaced

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Trends of valvular disease

Aortic and mitral disease are common; Pulmonic is not found in adults, but is commonly related to congenital heart disease in children; Tricuspid disease is very unusual in general

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Class I

Benefit >>> Risk, procedure/treatment SHOULD be performed/administered

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Class II

Benefit >> Risk, additional studies w/focused objectives needed; it is REASONABLE to perform procedure/administer treatment

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Class III

Benefit > Risk, additional studies w/broad objectives needed, additional registry data would help; procedure/treatment may be CONSIDERED

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Class IV

Benefit < Risk, no additional studies needed; procedure/treatment should NOT be performed/administered since it is NOT HELPFUL and may be HARMFUL

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Right Heart Failure

trouble breathing (SOB) when lying down, leg edema, crackles in lungs due to congestion, systolic hrt murmur more common, hrt will appear either dilated or hypertrophied on X-ray. L axis deviation

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Left Heart Failure

hard to diagnose at first. R axis deviation due to hypertrophied R ventricle, lungs are usually clear unless L hrt failure is also present, abdominal ascites due to hepatic portal congestion, jugular venous distension (JVD)

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Acute valvular disease

2 categories: Prosthetic valvular regurgitation (shock/heart failure) AND Infection (staph endocarditis = leaky valves)

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Subacute valvular disease

Subacute bacterial endocarditis (tired, SOB, fever, pains) OR Rheumatic heart disease (uncommon)

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Chronic valvular disease

Valvular heart disease can be compensated (what we want) or uncompensated

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Latent/indolent valvular disease

Mitral stenosis dt rheumatic heart disease from strep pyogenes as child (ask Jones Criteria; can develop pulmonary edema w/labor)

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Clinical manifestations

Abnml exam (murmurs; learn timing); dyspnea & fatigue (main Sx of heart failure); angina (typically aortic stenosis dt poor flow to heart muscle); syncope (pt can’t exercise/pass out); sudden cardiac death

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CXR

sees heart shadow, lung congestion, pericardium, aortic notch

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Angiogram

sees blood flow thru coronary aa, etc

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Echocardiogram

shows dynamic heart motion, valves, regurgitation, cardiac output

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Heart Catheter (Swan-Ganz)

shows pressures in different areas of venous blood flow and pulmonary capillary wedge pressure

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MRI

static image can show coronary arteries, pericardial fluid, aortic aneurysm

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Oxymetry

peripheral measurement at finger for O2 sat

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special angiograph techniques

transthoracic echocardiogram; transesophageal echo (can see vegetations of endocarditis)

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Congenital valvular diseases - “Collagen”

Ehlers-Danlos, Marfans, Pseudoxanthoma elasticum

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Rheumatic valvular diseases

Acute/latent/chronic; prophylasis for dental procedures; mitral valve usu involved (stenosis/insufficiency), aortic stenosis/insuff, or aortic stenosis; pulmonic is almost never involved

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Infectious valvular disease: acute

Staph aureus, sever illness, rapid destruction, surgery often needed, OPERATE immediately

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Infectious valvular disease: subacute

Strep viridans; vague/nonspecific illness; slowly progressive (months); antibiotics are main treatment

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Degenerative valvular disease: calcification

Cardiac fibroskeleton, aortic valve, mitral annulus

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Degenerative valvular disease: myxomatous change

Mitral vavle (single mitral valve replacement); aortic valve

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Mitral apparatus

Mitral valve leaflets, chordae tendineae, papillary muscles, left ventricle, mitral annulus, left atrium

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Murmur evaluation

Timing (systolic v. diastolic); Clicks (mitral - mid-diastolic); Snaps (mitral - diastolic; classic mitral stenosis inc intensity of S1); Character (ejection; crescendo/decrescendo; holosystolic; rumble; blowing (aortic regurgitation))

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Senile aortic stenosis

Presents in 70s-80s; fibrous encroachment; rigid; can’t open/close valve; normally very calcified

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Bicupsid aortic stenosis

Congenital anomaly; presents in 40s-60s

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Aortic stenosis

Valvular, Supravalvular (ring/web above; coarctation if close to subclavian); Subvalvular (membrane forms in L ventricular outflow track); Hypertrophic (muscular, cardiomyopathic illness)

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Aortic stenosis symptoms

None, dyspnea, angina, effort syncope, congestive heart failure

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Aortic stenosis signs

EKG (LVH, LBBB, LAE, LAD); Echo (LVH, LV size/fxn; AV/VLOT velocities, continuity equation - for a given valvular area measure velocity & that at stenotic location, modified Bernoulli equation, associated abnormalities)

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Aortic Insufficiency

Aorto-annular ectasia, bicuspid AV, calcific, rheumatic, infectious, HTN, dissection, marfans, trauma, seronegative spondylarthropathies, RA, arteritis, autoimmune; regurgitation is historically dt syphilis

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AI Symptoms

Well tolerated when young, dyspnea, nocturnal angina, palpitations

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AI Signs

Head bob, water hammer, nail bed pulsations, double pulse, fem booming pulses, systolic/diastolic bruits, pop BP > arm +60, uvula

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Mitral Stenosis

ECHO is best test!! Source of Arrhythmias; Require SBE prophylaxis (subacute bacterial endocarditis); Rheumatic, carcinoid, infiltrative, vegetations, neoplasm, mid-diastolic murmur

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Know all the diagnostic signs and that it can cause R hrt failure as well

Mitral facies, palpable S1, inc S1 loudness, inc P2, diastolic rumble w/presystolic accentuation, pulmonary HTN/RV failure, asymptomatic, dyspnea, adverse tachycardia, atrial arrhythmias, hemoptysis

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Mitral Valve Prolapse

Echocardiographic phenomenon; usu causes nothing; common in Marfans, Ehlers-Danlos; anxiety/fatigue/palpitations/orthostasis; neurocirculatory asthenia (chest pain that isn’t angina)

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Signs of MVP

Click-murmur; dynamic ausculatation, EKG, echo

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Mitral Regurgitation

80% are healthy; MR detected on Doppler; many etiologies; no Sx, but causes HF; may be dt disease of valve leaflets (ex: MVP or rheumatic mitral-valve disease), alterations fxn/structure of left ventricle dt ischemia or dilated cardiomyopathy

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Tricuspid Valve Disease

Regurgitation, stenosis (rare, exclusively rheumatic)

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28) Tricuspid Valve Disease: Signs and Sx

Right heart failure (ascities, hepato/splenomegaly, peripheral edema, systemic venous HT, Caravello’s sign (murmur is louder on inspiration = R heart prob); clear lungs

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