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Flashcard 150919457

Tags
#2015 #book-2 #cfa #cfa-level-1 #economics #schweser
Question
In the [...] run, if price is less than ATC, the firm has economic losses and will minimize losses in the [...] run by going out of business and reducing ongoing losses to zero.
Answer
long


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In the long run, if price is less than ATC, the firm has economic losses and will minimize losses in the long run by going out of business and reducing ongoing losses to zero.</

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ARIA is a developing standard that lets you supply extra information for screen readers through attributes on any HTML element.

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role attribute, which indicates the purpose of a given element.

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Contractility “ the inherent capacity of the myocardium to contract independently of changes in preload or afterload” Preload “the load present within the heart before contraction has started (i.e. at the end of diastole)” Afterload “the systolic load on the heart after it has started to contract; the sum of arterial blood pressure, aortic compliance, and obstructive lesions”

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Frank-Starling Mechanism “Increasing left ventricular preload will be matched by increases in stroke volume”

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Pathology of Aortic stenosis:
-congenital bicuspid valve
-degenerative (Ca & fibrosis restricts valve opening)
  • calcific (wear & tear)
  • ​rheumatic

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Pathophysiology

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Pressure Hypertrophy 13 Left ventricular pressure overload induces genes that promote concentric hypertrophy Concentric hypertrophy increases contractile force while normalizing wall stress… … but ultimately results in a “musclebound” heart that does not fill normally (diastolic dysfunction) and is unable to increase stroke volume in response to demand Critical aortic stenosis = fixed cardiac output

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Progression of aortic stenosis:
-50% reduction in valve orifice results in minimal pressure gradient
-Increments beyond this produce exponential increases in gradient
-Progression is variable between individuals
-Careful, frequent follow-up is important

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Angina Pectoris Syncope (especially effort-related syncope) Dyspnea (heart failure) 16

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Angina Pectoris 17 ↑Demand -left ventricular hypertrophy -myocardial O2 uptake - wall stress

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Syncope:
-Classically exertional
---Cardiac output is fixed and cannot rise with exercise
---Vasodilation occurs during exercise → Blood pressure & cerebral perfusion fall

-May also be from arrhythmia
---Tachycardia (ventricular or atrial)
---Bradycardia (heart block)

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Dyspnea Left ventricular hypertrophy diastolic dysfunction Progressive left ventricular dilation and contractile failure systolic dysfunction Signs and symptoms of heart failure (dyspnea on exertion, orthopnea, edema, pleural effusions)

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Sudden Death ~0.3% per year in the asymptomatic patient Mechanism = malignant tachy- or bradyarrhythmia

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Long asymptomatic “latent” period Onset of symptoms indicates a poor prognosis unless treated

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Possibile “Gallivardin’s dissociation

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AORTIC STENOSIS: SEVERITY

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A common congenital heart lesion ~1.5% of males, ~0.8% of females Prone to both aortic stenosis and regurgitation Associated with ascending aortic aneurysm, and a risk factor for aortic dissection Rarely associated with aortic coarctation (whereas the majority of instances of coarctation are associated with bicuspid aortic valves) At risk for aortic valve endocarditis 25

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Diagnosis ECG LA enlargement, LV hypertrophy Chest X-ray post stenotic aortic dilation, Ca ++ • Echocardiogram • Thickening and restricted motion of leaflets • Gradient and valve area can be calculated • Cardiac catheterization • Gradient across valve and valve area • Stress testing • For prognosis

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-Medical therapy for Aortic stenosis is basically non-existent
-Mechanical problem = mechanical treatment
-Afterload-reducing drugs are contraindicated
---BP = CO x resistance (by reducing resistance, BP will shoot down b/c CO can't increase to compensate)
-Mild to moderate asymptomatic aortic stenosis:
---Close follow up: history, exam, echocardiogram
---Warn re: endocarditis risk
---Treat associated atherosclerotic risk factors

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Why is aortic stenosis important? Common Major clinical implications Highly morbid once symptomatic Treatable

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Common Errors Failure to distinguish aortic sclerosis from stenosis Failure to diagnose and / or investigate Failure to act once symptoms arise Prescription of afterload-reducing drugs Abrupt reduction in preload / afterload (e.g. upon induction of a general anesthetic)

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aortic regurg:
Etiology Diseased valve cusps calcific degeneration, bicuspid, rheumatic Diseased aortic root hypertension with annulo-aortic ectasia, hereditary aortopathies, connective-tissue disorders, Marfan syndrome, syphilis Acute pathologies aortic dissection, trauma, endocarditis, prosthetic valve failure

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aortic regurg:
Pathophysiology - Acute Acute volume overload results in markedly elevated filling pressure The left ventricle does not have time to enlarge and accommodate Stroke volume rises modestly, inadequate to compensate for the regurgitant volume High left ventricular filling pressure is transmitted back to the left atrium, resulting in pulmonary congestion Forward cardiac output falls

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Pathophysiology - Chronic With time, genes are activated allowing increases in both left ventricular cavitary dimensions and wall thickness – described as eccentric hypertrophy or “cor bovinum” A very large total stroke volume allows forward output to remain normal; clinical features of wide pulse pressure are present The dilated ventricle accommodates larger volumes at a lower filling pressures, and pulmonary congestion is generally absent Ejection fraction remains normal during this phase May remain compensated for decades

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Chronic severe aortic regurgitation will eventually result in left ventricular fibrosis and systolic dysfunction

As the ventricle dilates further, wall tension and filling pressure rise

Ejection fraction falls, reducing stroke volume and forward output

Irreversible structural changes may occur prior to the development of symptoms
-one of the insidious features of regurgitation is that by the time sx's occur, you're already in big trouble

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Natural History

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Natural History Asymptomatic phase may last decades Adverse ventricular remodeling is often asymptomatic (initially) Symptoms associated with reduced left ventricular ejection fraction Exercise intolerance Dyspnea on exertion Angina (rare) Sudden death (rare)

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Palpitations – due to hyperdynamic stroke volume, heart interactions with the chest wall, and possibly extrasystoles Heart failure – dyspnea on exertion, orthopnea, peripheral edema, fatigue Angina Pectoris, Syncope (rare in isolated aortic regurgitation) 38

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Hyperdynamic precordium May radiate widely in a “sash” from R base to apex Associated with cardiomegaly and S 3 Multiple peripheral findings of large stroke volume

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Diagnostic Tests ECG - almost always shows LVH Chest x-ray - cardiomegaly Echocardiogram Cardiac catheterization

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Medical Management Surveillance Echocardiography follow LV size and function every few years if AR is mild, every 6-12 months if severe Avoid bradycardia – (prolonged diastole worsens regurgitation) Vigilance against endocarditis Diuretics - furosemide (Lasix) Vasodilators - nifedipine, ACE-inhibitors, hydralazine controversial - may reduce slope of decline in left ventricular function

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ndications for Surgical Management Definite Symptomatic with normal ejection fraction Symptomatic or asymptomatic with mildly decreased ejection fraction Very Probable Asymptomatic with normal ejection fraction but severe left ventricular dilation Probable Severe left ventricular systolic dysfunction

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Common Errors Failure to monitor for asymptomatic but irreversible adverse left ventricular remodeling Over-reliance on medications once symptoms or adverse remodeling occur

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Valve Surgery bioprosthetic valve mechanical valve

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Surgical Risks Peri-operative mortality ~ 2-4% for aortic valve replacement Mortality rate increases with: Age Poor left ventricular systolic function Associated valve disease Associated coronary artery disease Post-op prognosis fairly good Mechanical valve structural failure is rare Tissue valves eventually deteriorate

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Percutaneous Valve Intervention Balloon aortic valvuloplasty and trans-catheter aortic valve implantation

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Late Complications Systemic thromboembolism - 1- 2%/year (Less frequent in bioprosthetic valves) Mechanical valve thrombosis - 0.5%/year usually from inadequate anti-coagulation can be treated with thrombolysis or surgery Heart block Prosthetic valve endocarditis - 0.5- 1.0%/year

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Aortic stenosis → pressure overload
--“Concentric hypertrophy”
--Operate for symptoms

Aortic regurgitation → volume overload
--“Eccentric hypertrophy”
--Operate for adverse ventricular remodeling

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Etiology Almost always rheumatic (immunologic sequelae of Group A Streptococcal pharyngitis) Rheumatic fever usually occurs in childhood / adolescence Murmur appears ~ 20 years later Many don’t recall childhood illness Rheumatic valve disease is more common and progresses more rapidly in developing countries

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Etiology of mitral stenosis

Rare causes: Calcified mitral annulus, Atrial myxoma, Endocarditis, Carcinoid valvulopathy, Congenital

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Pathology – Rheumatic Mitral Stenosis Fibrotic, rigid mitral leaflets Fused valve commissures Short, thick, fused chordae tendinae Calcification of leaflets Aschoff nodules on histology

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Pathophysiology Obstruction to mitral inflow accentuates the pressure gradient from left atrium to left ventricle during diastole, resulting in elevated left atrial pressure Left atrial pressure overload causes: Pulmonary hypertension and interstitial / alveolar pulmonary edema due to back-transmission of pressure Left atrial dilation, resulting in 1. blood stasis and propensity for thromboembolism, and 2. risk of atrial fibrillation

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Now, all the people who visit your page get the enhanced experience with the pop up microformat button, no matter what browser they use.

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The second most popular microformat is hCalendar, a simple way of marking up events.

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Pathophysiology of mitral stenosis:

-A pulmonary capillary wedge pressure of 25mmHg causes transudation of fluid into alveoli, resulting in dyspnea

-Increases in pulmonary venous and capillary pressures raise pulmonary artery systolic pressure (pulm HTN)

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pulmonary hypertension right ventricular dilation tricuspid regurgitation ↑ pulmonary capillary wedge pressure R

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Severity Mild Moderate Severe Mean Gradient <5 mmHg 5-10 mmHg >10 mmHg Valve Area >1.5 cm 2 1.0-1.5 cm 2 <1.0 cm 2 Symptoms with vigorous exertion with activity with minimal activity * Gradients depend on diastolic filling time and cardiac output * Loss of atrial contraction e.g. in atrial fibrillation often results in marked worsening of symptoms

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Complications of mitral stenosis:

-Pulmonary edema & hemoptysis
-Atrial fibrillation and cardioembolism
-Right heart failure
-Endocarditis

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Flashcard 1343310400780

Question
The second most popular microformat is [...]
Answer
hCalendar, a simple way of marking up events.


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The second most popular microformat is hCalendar, a simple way of marking up events.

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Signs of pulmonary hypertension may coexist Inconspicuous LV apex Augmented S 1

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Flashcard 1343313022220

Question
The second most popular microformat is hCalendar, a simple way of marking up [...]
Answer
events.


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The second most popular microformat is hCalendar, a simple way of marking up events.

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ECG

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Flashcard 1343316430092

Question
What is microdata?
Answer
Microdata is a third take at solving the challenge of semantic markup.


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CXR Splayed carina Straight left heart border (pulmonary artery dilation and enlarged left atrial appendage) Pulmonary venous congestion

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Medical Therapies Reduce pulmonary congestion diuretics, e.g. furosemide Prevent / treat atrial fibrillation anti-arrhythmics, e.g. amiodarone Prevent embolism anticoagulation, e.g. coumadin Prevent / treat endocarditis oral hygiene early recognition & treatment

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New York Heart Association (NYHA) functional class:

I - no limitation
II - slight limitation, symptoms with ordinary activity
III - marked limitation, symptoms with less than ordinary activity
IV - symptoms at rest or any activity

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Indications for Intervention in mitral stenosis:

-Definite
---NYHA III-IV & valve area < 1.5 cm^2

-Very Probable
---Severe mitral stenosis (< 1.0 cm^2 ) & severe pulmonary hypertension (pulmonary artery pressure > 60-80 mmHg) & NYHA I-II

-Probable
---Asymptomatic patients with moderate or worse mitral stenosis (< 1.5 cm^2 ) with new onset atrial fibrillation

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Percutaneous Balloon Valvuloplasty

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Surgery for Mitral Stenosis

-Mechanical vs. bioprosthetic valves
---durability vs. anti-coagulation

-Mechanical valve thromboembolic complication rate ~ 3%/year

- ~30% of bioprosthetic mitral valves fail at 10 years

-mitral prostheses tend to last less than aortic ones b/c thrombotic rate is higher

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Etiology of mitral regurg:

-Leaflets/chordae
---Myxomatous (becomes progressively floppy), Rheumatic, Endocarditis (gets chewed up), Congenital

-Annulus
---Left ventricular dilation (cardiomyopathy)

-Papillary muscles
---Ischemia or infarction

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Pathophysiology of chronic mitral regurg

-A state of left ventricular and left atrial volume overload

-Left ventricular systolic function may remain normal for years until fibrosis and progressive dilation herald a decline in ejection fraction

-The low-pressure left atrial “outlet” is a form of afterload reduction - and may mask clinical deterioration
---Left ventricular ejection fraction may be normal despite impaired contractile function

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Pathophysiology of chronic mitral regurg:

-Reduced left ventricular ejection fraction in mitral regurgitation is serious... and indicates a poor prognosis regardless of treatment!

-When ejection fraction declines, diastolic filling pressures, left atrial & pulmonary pressures rise, Causing the left ventricle to dilate, increasing afterload further... creating more mitral regurgitation

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Pathophysiology (acute) Sudden volume overload Left ventricle and left atrium are not ready (no dilation, no hypertrophy) ↑ preload, ↓ afterload ↑ contractility (Frank-Starling mechanism, sympathetic activation) ↓ forward cardiac output, ↑ pulmonary capillary wedge pressure pulmonary edema, shock

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Acute vs. Chronic mitral regurgitation

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Clinical Features of mitral regurg:
-Fatigue
-Exertional dyspnea
-Orthopnea
-Edema
-Paroxysmal nocturnal dyspnea
-Palpitations

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Murmur PANsystolic - from S 1 to beyond S 2 • High gradient, high pitch • If severe, associated with S 3 and diastolic flow rumble Elevated left atrial pressure Cardiac apex is dilated and displaced May feel a thrill Lungs may be wet

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Diagnosis ECG Left atrial enlargement, left ventricular hypertrophy +/- atrial arrhythmias CXR Cardiomegaly, atrial dilation, pulmonary venous congestion Echocardiography Cardiac catheterization

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Medical Therapy of mitral regurg:

-Treat the underlying cause (if possible)
-Afterload reduction e.g. ACE inhibitors
---however, little if any benefit in delaying surgery (fundamental rx is surgery)
-Preload reduction: diuretics & nitrates
-Endocarditis recognition and treatment
-Anti-arrhythmics and anti-coagulants (for complications)

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Surgical Therapy (mitral regurg)

-Valve repair:
---for myxomatous degeneration / prolapse; less successful in other etiologies
---good outcomes in selected patients
---preferable

-Valve replacement: Mechanical vs. bioprosthetic

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Indications for Surgery Definite Acute symptomatic mitral regurgitation NYHA II-IV & normal ventricular function Symptomatic or not with left ventricular systolic dysfunction Surgery is relatively contraindicated in the context of severe ventricular dysfunction

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Surgical Outcomes Operative mortality ~ 6% Repair associated with: Better long-term survival Greater freedom from thromboembolism Less risk of bleeding Less risk of endocarditis Long-term outcomes are related to underlying cause

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Mitral stenosis → Lt ventricular underfilling, pulm edema
-Balloon or surgery for symptoms

Mitral regurgitation → Left ventricular volume overload
-Operate for adverse ventricular remodeling or symptoms

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Transient Bacteremia (exposure) + Predisposing Cardiac Lesion (diathesis) (abn leaky flow, turbulent flow, etc) = Infective Endocarditis

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Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival & nailbed hemorrhages, Janeway lesions (painless, on hands and feet) Immunological phenomena: glomerulonephritis, Roth spots (retinal infarcts), positive rheumatoid factor, Osler’s nodes (painful, on hands and feet),

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Modified Duke Criteria for Endocarditis Major Criteria Positive blood cultures with typical organism Evidence of endocardial involvement (by echocardiography) Minor Criteria Predisposition Fever Vascular phenomena Immunologic phenomena Microbiological evidence

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Treatment of Endocarditis:

-Targeted parenteral animicrobial therapy
---Narrow-spectrum, intensive, synergistic
---Depends on culture and sensitivity!
-Eliminate portal of entry (if possible)
-Valve surgery
---For hemodynamic compromise
---For recurrent embolism
---For large and highly mobile vegetations
---For prosthetic valve endocarditis
---For fungal endocarditis

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Common Errors Failure to recognize asymptomatic left ventricular dysfunction in the context of mitral regurgitation Failure to anticoagulate for atrial fibrillation in the context of rheumatic mitral stenosis Failure to provide bridging anticoagulation for mechanical valvular prostheses Failure to recognize and treat infective endocarditis

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Choosing Wisely It is cost-ineffective, unwarranted, and / or inadvisable to perform routine echocardiography in: Asymptomatic patients with innocent murmurs Asymptomatic patients with mild aortic stenosis more often than every 3-5 years Asymptomatic patients with mild mitral regurgitation and normal ventricular size and function

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Aortic stenosis → pressure overload “Concentric hypertrophy” Operate for symptoms Aortic regurgitation → volume overload “Eccentric hypertrophy” Operate for adverse ventricular remodeling

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Mitral stenosis → Balloon or surgery for symptoms Mitral regurgitation → Left ventricular volume overload Operate for adverse ventricular remodeling or symptoms

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Cardiac Valve Surgery Durability v.s. thromboembolic risk Replacing one disease with another Endocarditis Clinical manifestations and diagnostic criteria Exposure + Diathesis model Prophylaxis guidelines

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Article 1343376985356

History of the United States
#has-images

History of the United States From Wikipedia, the free encyclopedia "American history" redirects here. For the history of the continents, see History of the Americas. Part of a series on the History of the United States Timeline[hide] Prehistory Pre-Colonial Colonial period 1776–1789 1789–1849 1849–1865 1865–1918 1918–1945 1945–1964 1964–1980 1980–1991 1991– present By ethnicity[show] By topic[show] United States portal v t e The date of the start of the history of the United States is a subject of debate among historians. Older textbooks start with the arrival of Christopher Columbus in 3 August 1492 and emphasize the European background, or they start around 1600 and emphasize the American frontier. In recent decades American schools and universities typically have shifted back in time to include more on the colonial period and much more on the prehistory of the Native peoples. [1] [2] Indigenous people lived in what is now the United State