Insuficienta cardiaca1

8/13/2019 Insuficienta cardiaca1

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Learning Objectives

Following this presentation, the participant shouldbe able to:1. Recognize the magnitude of heart failure epidemic and its public health

implications2. Distinguish the different classifications and stages of heart failure

3. Review underlying pathophysiology of heart failure

4. Discuss signs and symptoms of heart failure exacerbation

5. Identify current practice guidelines for treatment of acute decompensatedheart failure


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Definition Heart failure occurs when the heart cannot pump

enough blood fast enough to meet the metabolicneeds of the body.

No longer use the term congestive because all heartfailure does not result in clinically apparent volumeoverload


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Epidemiology Estimated that over 5 million Americans have heart failure

Estimated 500,000 new cases per year

Within 5 years, half of those diagnosed will be dead

Over 1 million hospitalizations per year with HF as primarydiagnosis

Most common reason for hospitalization in those >65 yearsold

85% of HF cases are in adults 65 and older Heart failure is 4th in a list of quality of care initiatives in

vulnerable older adults


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Costs of Heart Failure

It is the leading cause of hospitalization in patients older than 65 years ofage and is a primary hospital discharge diagnosis in 1.1 million people ofall ages each year.

It is one medical condition for which mortality continues to increase.From 1994 to 2004, the overall death rate declined 2.0% in the UnitedStates, but deaths from HF increased 28% in the same time period.

According to the National Heart, Lung, and Blood Institute, theestimated direct and indirect costs associated with HF care in the US is$33.2 billion yearly.

The majority of the costs approximately two-thirds are attributable tothe management of episodes of acute HF decompensation (i.e.,hospitalization).


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Different Ways to Define HF - 1 Dilated (congestive) cardiomyopathy is a group of heart muscle

disorders in which the ventricles enlarge but are not able to pumpenough blood for the body's needs, resulting in heart failure.(Example - CAD, myocarditis, EtOH, HIV)

Hypertrophic cardiomyopathy includes a group of heart disorders inwhich the walls of the ventricles thicken (hypertrophy) and becomestiff, even though the workload of the heart is not increased.(Example congenital HOCM, or acquired)

Restrictive (infiltrative) cardiomyopathy includes a group of heart

disorders in which the walls of the ventricles become stiff, but notnecessarily thickened, and resist normal filling with blood betweenheartbeats. (Example radiation, amyloidosis)


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Different Ways to Define HF - 2Diastolic Versus Systolic Heart Failure

A. Systolic cardiac (heart) dysfunction (or systolic heart

failure) occurs when the heart muscle doesn'tcontract with enough force, so there is not enoughoxygen-rich blood to be pumped throughout thebody.

B. Diastolic cardiac dysfunction (or diastolic heartfailure) occurs when the heart contracts normally,but the ventricle doesn't relax properly so less bloodcan enter the heart.


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Different Ways to Define HF - 3 Clinically, patients are classified as having HF ofischemic or nonischemic etiology based on a historyof myocardial infarction (MI) or based on objectiveevidence of coronary artery disease (CAD) such asangiography or functional testing.


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Controversial Definitions


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Etiology Underlying causes: Underlying causes of heart failure include

structural abnormalities (congenital or acquired) that affect theperipheral and coronary arterial circulation, pericardium,myocardium, or cardiac valves, thus leading to increasedhemodynamic burden or myocardial or coronary insufficiency

Fundamental causes: Fundamental causes include the biochemical

and physiologic mechanisms, through which either an increasedhemodynamic burden or a reduction in oxygen delivery to themyocardium results in impairment of myocardial contraction

Precipitating causes: Overt heart failure may be precipitated byprogression of the underlying heart disease (eg, further narrowing of a

stenotic aortic valve or mitral valve) or various conditions (fever,anemia, infection) or medications (chemotherapy, NSAIDs) that alterthe homeostasis of heart failure patients

Genetics of cardiomyopathy: Dilated, arrhythmic right ventricular andrestrictive cardiomyopathies are known genetic causes of heart failure.


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Underlying causes - 1

Systolic heart failure Diastolic heart failure Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (stenosis or regurgitantlesions)

Arrhythmia (supraventricular or ventricular)

Infections and inflammation (myocarditis)

Peripartum cardiomyopathy

Congenital heart disease

Drugs (either recreational, such as alcohol andcocaine, or therapeutic drugs with cardiac sideeffects, such as doxorubicin)

Idiopathic cardiomyopathy

Rare conditions (endocrine abnormalities,rheumatologic disease, neuromuscular

conditions)

Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (aorticstenosis)

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy

(amyloidosis, sarcoidosis)

Constrictive pericarditis


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Acute heart failure High-output heart failure

Acute valvular (mitral oraortic) regurgitation

Myocardial infarction Myocarditis

Arrhythmia

Drugs (eg, cocaine, calciumchannel blockers, or beta-blocker overdose)

Sepsis

Anemia

Systemic arteriovenous fistulas

Hyperthyroidism

Beriberi heart disease

Paget disease of bone

Albright syndrome (fibrousdysplasia)

Multiple myeloma

Pregnancy

Glomerulonephritis

Polycythemia vera

Carcinoid syndrome


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Right heart failure

Left ventricular failure

Coronary artery disease (ischemia) Pulmonary hypertension

Pulmonary valve stenosis

Pulmonary embolism

Chronic pulmonary disease Neuromuscular disease


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Precipitating causes The most common cause of decompensation in a previously

compensated patient with heart failure is inappropriate reduction inthe intensity of treatment, such as dietary sodium restriction,physical activity reduction, or drug regimen reduction

Uncontrolled hypertension is the second most common cause ofdecompensation, followed closely by cardiac arrhythmias (mostcommonly, atrial fibrillation)

Systemic infection or the development of unrelated illness can alsolead to heart failure

Cardiac infection and inflammation can also endanger the heart.Myocarditis or infective endocarditis may directly impair myocardialfunction and exacerbate existing heart disease

Intense, prolonged physical exertion or severe fatigue, such as mayresult from prolonged travel or emotional crisis, is a relatively commonprecipitant of cardiac decompensation

Excessive intake of water and/or sodium and the administration ofcardiac depressants or drugs that cause salt retention are other factorsthat can lead to heart failure


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Causes of Heart Failure Coronary artery disease Problems with the heart muscle itself [known as

cardiomyopathy (myocarditis, etc)]

Hypertension Problems with any of the heart valvesAbnormal heart rhythms (also called arrhythmias) Toxic substances (EtOH, cocaine)

Congenital heart disease Diabetes Thyroid problems HIV


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Diastolic HF (heart failure with

normal ejection fraction-HFNEF)Diastolic heart failure is defined as a condition caused by increased resistance to thefilling of one or both ventricles; this leads to symptoms of congestion from theinappropriate upward shift of the diastolic pressure-volume relation.

40% of patients Increasing incidence with age

More common in women

HTN and cardiac ischemia are most common causes

Common precipitating factors include volume overload; tachycardia; exercise;hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection,thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodalblock); increased salt intake; and use of nonsteroidal anti-inflammatory

drugs.


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Diastolic Dysfunction Alterations involve relaxation and/or filling

and/or distensibility.

Arterial hypertension associated to LVconcentric remodelling is the maindeterminant of DD but several other cardiacdiseases, including myocardial ischemia, andextra-cardiac pathologies also possible.


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Stages of Diastole1.Isovolumetric relaxation, period occurring between the end of LVsystolic ejection (= aortic valve closure) and the opening of the mitralvalve, when LV pressure keeps going its rapid fall while LV volumeremains constant.

2. LV rapid filling, which begins when LV pressure falls below left atrialpressure and the mitral valve opens. During this period the blood has anacceleration which achieves a maximal velocity, direct related to themagnitude of atrio-ventricular pressure, and stops when this gradientends.

3. diastasis, when left atrial and LV pressures are almost equal and LVfilling is essentially maintained by the flow coming from pulmonary veins

with left atrium representing a passive conduit

with an amountdepending of LV pressure, function of LV "compliance".

4. atrial systole, which corresponds to left atrial contraction and ends atthe mitral valve closure. This period is mainly influenced by LVcompliance, but depends also by the pericardial resistance, by the atrialforce and by the atrio-ventricular synchronicity (= ECG PR interval).


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Patient Differences HF is a hemodynamic disorder but there is a

poor relationship between measures of cardiac

performance and patient symptoms For example, pts with very low EF may be

asymptomatic while someone with preservedEF may be severely disabled with symptoms


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Body Compensatory Mechanisms Epinephrine and norepinephrine release which increases heart rate and

contractility which increased myocardial work load

Decrease salt and water excretion from kidneys which helps maintain BPby increasing blood volume, this leads to stretching of hearts chambers

which can impair ability to contract Hypertrophy and thickening of heart muscle which initially increases

contractility but over time leads to stiff chambers and can impaircontractility

HF patients have higher levels of epinephrine, norepinephrine,

aldosterone, angiotensin II, endothelin, inf lammatory cytokines, andvasopressin which contribute to heart remodeling, progression of HF, andhigher levels are associated with increased mortality


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Potential Reasons

Alternation in ventricular distensibility

Valvular regurgitation

Pericardial restraint Cardiac rhythm

Conduction abnormalities

RV function

Also several non-cardiac factors including peripheralvascular fxn, reflex autonomic activity, renal sodiumhandling, etc.


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Cardiovascular Medical History Hx of heart failure

Angina

MI

CABG

PCI

Pacemaker/ICD

Embolic events

arrhythmias

CVA

PVD

Rheumatic Dx

Other valvular hx

Congenital


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Signs and symptoms Exertional dyspnea and/or

dyspnea at rest Orthopnea Acute pulmonary edema Chest pain/pressure and

palpitations Tachycardia Fatigue and weakness Nocturia and oliguria Anorexia, weight loss, nausea Exophthalmos and/or visible

pulsation of eyes Nausea Abdominal Fullness

Distention of neck veins Weak, rapid, and thready

pulse Rales, wheezing S3 gallop and/or pulsus

alternans Increased intensity of P2

heart sound Hepatojugular reflux

Ascites, hepatomegaly,and/or anasarca

Central or peripheralcyanosis, pallor

Edema


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Signs and SymptomsSign or Symptom + Why It Happens + People with Heart Failure May Experience...

1. Shortness of breath or dyspnea

A. Blood "backs up" in the pulmonary veins because theheart can't keep up with the supply. This causesfluid to leak into the lungs

a. Breathlessness during activity (most commonly), atrest, or while sleeping, which may come on

suddenly and wake them up. They often havedifficulty breathing while lying flat and may needto prop up the upper body and head on two pillows.They often complain of waking up tired or feelinganxious and restless.


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More Signs and Symptoms2. Persistent coughing or wheezing

A. Fluid builds up in the lungs

a. coughing that produces white or pinkblood-tinged mucus.

3. Lack of appetite of nausea

A. Digestive system receives less blood

causing problems with digestion

a. Full feeling, early satiety, nausea


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Additional Signs4. Confusion, impaired thinking

A. Changing levels of certain substances in the blood,such as sodium, can cause confusion..

a. memory loss and feelings of disorientation. Acaregiver or relative may notice this first.


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More Signs & Symptoms5. Increased heart rate

A. To "make up for" the loss in pumpingcapacity, the heart beats faster.. . .

a. heart palpitations, which feel like theheart is racing or throbbing.

6. More symptoms weight gain, frequent urination,

cough, decreased physical activity


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Physical ExaminationSigns that suggest heart failure include:

1. Tachycardia

2. Third heart sound (S3) (LISTEN LL RECUMBANT)3. Increased jugular venous pressure

4. Positive hepatojugular reflux

5. Bilateral rales (not always present)

6. Peripheral edema not due to venous insufficiency

7. Laterally displaced apical impulse

8. Weight gain


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HF Diagnosis and Assessment Remains primarily a clinical diagnosis but additional

information via other diagnostics can be beneficial

Evaluation depends on if this is first presentation,change in clinical symptoms, certainty of diagnosis,etc


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DiagnosisHeart failure criteria, classification, and staging

The Framingham criteria (2 major criteria or1 major and 2 minor criteria)

Major criteria Minor criteria

Paroxysmal nocturnal dyspnea Weight loss of 4.5 kg in 5 days in

response to treatment Neck vein distention Rales Acute pulmonary edema Hepatojugular reflux S3 gallop

Central venous pressure greaterthan 16 cm water Circulation time of 25 seconds Radiographic cardiomegaly Pulmonary edema, visceral

congestion, or cardiomegaly at

autopsy

Nocturnal cough

Dyspnea on ordinary exertion

A decrease in vital capacity byone third the maximal valuerecorded

Pleural effusion

Tachycardia (rate of 120 bpm)

Bilateral ankle edema


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The New York Heart Association (NYHA)

classification Class I: No limitation of physical activity

Class II: Slight limitation of physical activity

Class III: Marked limitation of physical activity Class IV: Symptoms occur even at rest; discomfort with

any physical activity


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The American College of Cardiology/American

Heart Association (ACC/AHA) staging system Stage A: High risk of heart failure but no structural

heart disease or symptoms of heart failure

Stage B: Structural heart disease but no symptoms ofheart failure

Stage C: Structural heart disease and symptoms ofheart failure

Stage D: Refractory heart failure requiring specializedinterventions


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High Risk for Developing HFHypertension

CADDiabetes mellitus

Family history of cardiomyopathy

Asymptomatic HFPrevious MI

LV systolic dysfunctionAsymptomatic valvular disease

Symptomatic HFKnown structural heart diseaseShortness of breath and fatigue

Reduced exercise tolerance

RefractoryEnd-Stage HF

Marked symptoms at restdespite maximal

medical therapy

A

B

CD


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ACC/AHA staging system

Level Description Examples Notes

A At high risk for heart failure but

without structural heart diseaseor symptoms of heart failure

Patients with coronary artery

disease, hypertension, ordiabetes mellitus withoutimpaired LV function,hypertrophy, or geometricchamber distortion

Patients with predisposing risk

factors for developing heartfailureCorresponds with patients withNYHA class I heart failure

B Structural heart disease butwithout signs/symptoms of

heart failure

Patients who are asymptomaticbut who have LVH and/or

impaired LV functionC Structural heart disease with

current or past symptoms ofheart failure

Patients with known structuralheart disease and shortness ofbreath and fatigue, reducedexercise tolerance

The majority of patients withheart failure are in this stageCorresponds with patients withNYHA class II and III heartfailure

D Refractory heart failure requiringspecialized interventions

Patients who have markedsymptoms at rest despite

maximal medical therapy

Patients in this stage may beeligible to receive mechanical

circulatory support, receivecontinuous inotropic infusions,undergo procedures to facilitatefluid removal, or undergo hearttransplantation or otherproceduresCorresponds with patients withNYHA class IV heart failure


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Staging of Heart Failure


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Diagnosis

Testing - Laboratory studies Complete blood count (CBC) Urinalysis Electrolyte levels Renal and liver function studies

Fasting blood glucose levels Lipid profile Thyroid stimulating hormone (TSH) levels B-type natriuretic peptide levels N-terminal pro-B-type natriuretic peptide

Electrocardiography Chest radiography 2-dimensional (2-D) echocardiography Nuclear imaging Maximal exercise testing

Pulse oximetry or arterial blood gas


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Laboratory tests Complete blood count (CBC), which may indicate anemia or infection as

potential causes of heart failure Urinalysis (UA), which may reveal proteinuria, which is associated with

cardiovascular disease Serum electrolyte levels, which may be abnormal owing to causes such as f luid

retention or renal dysfunction Blood urea nitrogen (BUN) and creatinine levels, which may indicate

decreased renal blood flow Fasting blood glucose levels, because elevated levels indicate a significantly

increased risk for heart failure (diabetic and nondiabetic patients) Liver function tests (LFTs), which may show elevated liver enzyme levels and

indicate liver dysfunction due to heart failure

B-type natriuretic peptide (BNP) and N-terminal pro-B-type (NT-proBNP)natriuretic peptide levels, which are increased in heart failure; thesemeasurements are closely correlated with the NYHA heart failure classification

Electrocardiogram (ECG) (12-lead), which may reveal arrhythmias,ischemia/infarction, and coronary artery disease as possible causes of heartfailure


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Imaging studies Chest radiography (posterior-anterior, lateral), which may show pulmonary congestion,

an enlarged cardiac silhouette, or other potential causes of the patient's symptoms

2-D echocardiographic and Doppler flow ultrasonographic studies, which may revealventricular dysfunction and/or valvular abnormalities[62, 63]

Coronary arteriography in patients with a history of exertional angina or suspectedischemic LV dysfunction, which may reveal coronary artery disease

Maximal exercise testingwith/without respiratory gas exchange and/or blood oxygensaturation, which assesses cardiac and pulmonary function with activity, the inability to

walk more than short distances, and a decreased peak oxygen consumption reflect moresevere disease


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Other studies

Screening for hemochromatosis, in which iron overload affectscardiac function Screening for sleep-disturbed breathing, which affects

neurohormonal activation Screening for human immunodeficiency virus (HIV), which may

result in heart failure from possible direct infectious effects, from

disease treatment effects causing CAD, or from other causes Testing for rheumatologic diseases, amyloidosis, or

pheochromocytoma, all of which may cause cardiomyopathy Serum and urine electrophoresis for light-chain disease Genetic testing for at-risk patients with a first-degree relative who

has been diagnosed with a cardiomyopathy leading to heart failure,which may aid in detecting early disease onset and guide treatment Holter monitoring, which may reveal arrhythmias or abnormal

electrical activity (eg, in patients with heart failure and a history of MIwho are being considered for electrophysiologic study to documentventricular tachycardia [VT] inducibility)


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B-type natriuretic peptide (BNP) and N-terminal pro-B-type

natriuretic peptide (NT-proBNP) levels to use or not

- Can be useful in differentiatingcardiac and noncardiac causes ofdyspnea

- Elevated BNP levels have beenassociated with reduced LVEF,LVH, elevated LV fillingpressures, and acute MI- Evidence supports baselinelevels for acute exacerbations atthis time- Evaluation with coronaryangiography on initial dx orpresentation is recommended


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What We Should Know about the

Individual Patients HF1. Identify the patients with HF2. Assess for S/S and risk factors for HF3. Initial work up should have been included work up for

reversible causes if appropriate (TSH, HIV, etc.)4. Echocardiogram to determine systolic and diastolic LV

performance, cardiac output (ejection fraction), andpulmonary artery and ventricular filling pressures

5. Chest X-ray to help identify vascular congestion,infiltrates, effusions

6. Evaluation and classification of severity of heart failure

7. Nuclear imaging for assessment of ejection fraction orareas of ischemia (as appropriate)


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Acute HFIn acute heart failure, patient care consists of: stabilizing the patient's clinical condition;

establishing the diagnosis, etiology, and precipitatingfactors;

initiating therapies to provide rapid symptom reliefand survival benefit


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Management of HFNonpharmacologic

therapyPharmacotherapy

Oxygen andnoninvasive positivepressure ventilation,

Dietary sodium andfluid restriction,

Physical activity asappropriate,

Attention to weightgain

Diuretics,

Vasodilators,

Inotropic agents, Anticoagulants,

Beta blockers,

Digoxin

Modern therapy

Electrophysiologicintervention

Revascularization

procedures Valve

replacement/repair

Ventricular restoration

Extracorporeal

membraneoxygenation

Ventricular assistdevices

Heart transplantation

Total artificial heart


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Non-pharmacologic therapy


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Management/TreatmentPharmacotherapyA. Loop diuretics [furosemide (THRESHOLD DRUG),

bumentanide, torsemide] to treat volumeoverload may add metolazone to any

NO EFFECT ON MORTALITY

B. Management of systolic dysfunction with an ACE

inhibitor like captopril, lisinopril1. Main side effects cough, hyperkalemia,

angioedema, orthostasis


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Management/TreatmentC. B-blocker such as carvedilol, metoprolol XL,***GOAL DOSES

D. Addition of ARB may be substituted for ACE-I

E. Spironolactone for patients with Stage III or IV heart failure,the RALES trial

** Watch for hyperkalemia

F. Digoxin helps with morbidity not mortality

**10-18% of nursing home pts develop toxicitySide effects include arrhythmias, visual changes, GIcomplaints, altered mental status

G. Nitrates and Hydralazine particularly in African Americans

h h


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Pharmacotherapy Diuretics (to reduce edema by reduction of blood volume and venous pressures) and

salt restriction (to reduce fluid retention) in patients with current or previous heartfailure symptoms and reduced left ventricular ejection fraction (LVEF) forsymptomatic relief

Angiotensin-converting enzyme inhibitors (ACEIs) for neurohormonalmodification, vasodilatation, improvement in LVEF, and survival benefit

Angiotensin receptor blockers (ARBs) for neurohormonal modification,vasodilatation, improvement in LVEF, and survival benefit

Hydralazine and nitrates to improve symptoms, ventricular function, exercise

capacity, and survival in patients who cannot tolerate an ACEI/ARB or as an add-ontherapy to ACEI/ARB and beta-blockers in the black population for survival benefit Beta-adrenergic blockers for neurohormonal modification, improvement in

symptoms and LVEF, survival benefit, arrhythmia prevention, and control ofventricular rate

Aldosterone antagonists, as an adjunct to other drugs for additive diuresis, heartfailure symptom control, improved heart rate variability, decreased ventricular

arrhythmias, reduction in cardiac workload, improved LVEF, and increase in survival Digoxin, which can lead to a small increase in cardiac output, improvement in heart

failure symptoms, and decreased rate of heart failure hospitalizations Anticoagulants to decrease the risk of thromboembolism Inotropic agents to restore organ perfusion and reduce congestion


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Basic Pharmacotherapy for HFpatients

All patients with systolic heart failure should be on ACE-I and -blockersunless contraindications are present (ARBs can substitute if there isintolerance to these drug classes, i.e.: ARBs can be used in combination

with ACE-I or with blockers).

Concerns about blood pressure may occur as these drugs are titratedupwards limitations should relate to symptoms of low BP rather thanactual BP values (for systolic BP above 80 mm Hg) so persistence with thetitration should occur unless such symptoms occur. Concerns about renalfunction may occur as these drugs are titrated upwards.


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Electrolytes

Please remember that many of these medicationshave severe impacts on patients electrolyte panels.

Check electrolytes on a regular basis in patientswith heart failure

Have open communication with your physiciansregarding medications/plans of care for your HF

patients.


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Role of RAS in HF


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Role of ACE-I


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ARBs

Angiotensin receptor blockers act as antagonist at theAT1 receptor

Many ARBs have been proven beneficial as alternativeto ACE-I in HF treatment and prevention

Some studies suggest concurrent use has additionalbenefit


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COST OF HEART FAILURE

Researchers found that five years of treatmentfor heart failure without beta-blockers cost atotal of $52,999.

With beta-blockers added to treatment, totaltreatment costs fell by $3,959, patient survivalincreased by an average of about three-and-a-

half months, and patients needed fewerovernight hospital stays.


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Tolvaptan


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Initial Data on TolvaptanTolvaptan added to standard meds rapidly lowered body weight, and the weightwas kept off during therapy.

Low doses were as effective as higher doses.

Tolvaptan did not lower blood pressure or change blood levels of potassium,BUN or creatinine (it did not reduce kidney function).

Tolvaptan brought low blood sodium levels back up to normal.

Tolvaptan did not worsen heart failure (risk of death, rehospitalization, andunscheduled visits for CHF).

There was a trend toward lower mortality in tolvaptan patients with seriouscongestion, low blood sodium, or weak kidney function.

The greatest benefit with tolvaptan is seen in the sickest patients.
http://www.chfpatients.com/tests/routine_tests.htmhttp://www.chfpatients.com/tests/routine_tests.htm


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Inpatient vs Outpatient Management

Nesiritide is a new drug that is a synthetic BNP thatvasodilates vessels and serves as a potent diuretic agent

Inotropic agents (dobutamine, milrinone) often

used inpt, potent inotropic agents used to increasecardiac output use is controversial in outpt settings,may improve morbidity, definite use in hospice setting,increase risk of arrhythmias which is important inthose with AICDs


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Modern therapy

1) Devices: Left ventricular assisted device (LVAD),

Cardiac resynchronization therapy (CRT)

Internal cardiac defibrillator (ICD)

2) Surgery: Heart valve surgery (Valve replacement/repair),

Revascularization procedures

Infarct exclusion surgery - Modified Dor or DorProcedure)

3) Extracorporeal Membrane Oxygenation (ECMO)

4) Heart transplant

5) Total Artificial Heart (TAH)


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Devices - Implantable cardioverter-

defibrillators (ICD) Patients with LV dysfunction (LVEF 35%) from a previous MI

who are at least 40 days post-Ml Patients with nonischemic cardiomyopathy; with an LVEF 35 %;

in NYHA class II or III; receiving optimal medical therapy; and

expected to survive longer than 1 year with good functional status Patients with ischemic cardiomyopathy who are at least 40 days

post-MI; have an LVEF 30%; are in NYHA functional class I; areon chronic optimal medical therapy; and are expected to survivelonger than 1 year with good functional status

Patients who have had ventricular fibrillation (VF) Patients with documented hemodynamically unstable ventricular

tachycardia (VT) and/or VT with syncope; with an LVEF less than40%; on optimal medical therapy; and expected to survive longerthan 1 year with good functional status


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What is an ICD?

Laymens definition:

The abbreviation for automatic internal cardiacdefibrillator, an amazing device that is often

implanted in individuals suffering from Iife-threatening disordered heart beating.

The AICD device is able to deliver a jolt ofelectricity to an abnormally beating heart; the

shock restores normal orderly heart beating.Thus, on its own, this device is able to ward offsudden death.


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High Tech Devices

These devices are designed to pick up lethalheart rhythms such as ventricular fibrillationand ventricular tachycardia and deliver an

appropriate shock However, if atrial fibrillation or other

supraventicular tachycardias go fast enoughand look a certain way to the computer it will

shock fast afib Pt often describes a mule kicking them in the

chest feeling


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Devices - Cardiac resynchronization

therapy/biventricular pacing (CRT) Patients in sinus rhythm or atrial fibrillation with a QRS

120 ms (the greatest benefit is in patients with a QRS >150ms) and an LVEF


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Guidelines for CRTAn estimated one-third of patients with low EF and class III to IV symptoms of

HF manifest a QRS duration >120 ms.


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Devices - Left ventricular assisted

device (LVAD)Survival for women 62% versus 78.5% for men

Women present later for LVAD evaluation

Newer devices are smaller and now better designed forwomen

Provide either partial (parallel pump) or full (ventricular

bypass) systemic and/or pulmonary perfusion


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Definition A ventricular assist device (VAD) is a mechanical pump

used for temporary blood circulation support. It decreasesthe workload of the heart while maintaining adequate flow

and blood pressure. A VAD is a temporary life-sustaining device. VADs can

replace the left ventricle (LVAD), the right ventricle(RVAD), or both ventricles (BIVAD). They are used whenthe heart muscle is damaged and needs to rest in order to

heal or when blood flow from the heart is inadequate.VADs can also be used as a bridge in patients awaitingheart transplantation or in patients who have rejected atransplanted heart.


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Example of one VADdevice:HeartMate Implantable

h VA i f


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The VAD consists of: A pump unit, implanted in the abdomen (location of placement is based on the patient's

past medical history, anatomy and surgeon preference)

An inflow tube (or conduit), attached to the bottom of the left ventricle (apex)

An outflow tube, attached to the aorta (the large artery that carries blood away from yourheart)

Internal valves that allow for one-way blood flow through the system

Power leads, that pass from the internal device through the skin, and outside your body.The outside of the tube is covered with a special material so that skin cells grow into thematerial and aids healing.

External controller and power base unit or battery pack that attaches to the powerleads/cables. The controller is programmed to maintain a specific pump spread. It displaysthe status of the system and any alarm messages, and also sounds alarms if needed. The

batteries are rechargeable and changed daily.

The controller and batteries can be worn in a belted waist pack or a holster under thearm. Or, it may be connected to a power base unit and plugged into a wall outlet.

The type of pump and other components depends on the type of VAD used


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Patients who might be candidates for a VAD: have suffered a massive heart attack

cannot be weaned from heart-lung bypass after treatmentwith intravenous fluids, medications, and insertion of a

balloon pump in the aorta have an infection in the heart wall that does not respond to

conventional treatment

are awaiting a heart transplant and are unresponsive todrug therapy and intravenous fluids

are undergoing high-risk procedures to clear the blockagesin a coronary artery


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Poor candidates for a VAD:

irreversible renal failure severe disease of the vascular system of the brain cancer that has spread (metastasized) severe liver disease

blood clotting disorders severe lung disease infections that do not respond to antibiotics extreme youth or age


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Types of VADs There are 4 types of VADs, each appropriate for a differentcondition.

Surgery to install a VAD is performed under general anesthesia

in a hospital operating room. An incision is made in the chest, then catheters are inserted

into the heart and the correct artery.

The surgeon sutures the catheters in place, then attachestubing to connect the catheters to the pump.

The pump stays outside the body. Once it is turned on, blood flows out of the diseased ventricle

and into the pump, then is returned to the correct blood vesselleaving the heart.


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Technique Blood is passively drained via a large cathater from

either the left atrium or left ventricle, passes through

the pump chamber and is returned via an outflow

catheter to the aorta.

Cannula placement varies according to the surgery,

the pump being used and the ventrical(s) being

supported.


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Ideal requirements1. Durable2. Biocompatible

3. Nonthrombogenic4. Resistant to infection

5. Reasonably priced

6. Available numerous size


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Classification of VADs:

Centrifugal (BioMedicus, Sarns Delphin)

Non-pulsatile Rotary (Hemopump) Pulsatile pneumatic (Thoratec, ABIOMED BVS 5000,

Symbion AVAD)

Pulsatile pneumatic implantable (TCI Heartmate) Pulsatile electrical implantable (Novocor LVAS, TCI

Heartmate)

type of pump used ventrical assisted (LVAD vs RVAD vs BVAD)

BVAD vs TAH


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Recent available specifications

Centrifugal pump Implantable pneumatic pulsatile Heartmate

(Thermo Cardiosystem)

Paracorporeal ABIOMED BVS 5000 pump(ABIOMED) Paracorporeal pneumatic pulsatile Thoratec VAD

(Thoratec Laboratories)

Paracorporeal pulsatile pediatric VAD Systemincluding Berlin Heart VAD (MediportKardiotechnik) & MEDOS HIA-VAD System(BYTEC GmbH)

Jarvik 2000 System (Jarvik Research)

List of implantable VAD devicesD i M f t


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Device Manufacturer Type Approval Status as of July 2012

Novacor World Heart Pulsatile.

Was approved for use in North America, European Union

and Japan. Now defunct and no longer supported by the

manufacturer. (Heartware completed acquisition August

2012)

HeartMate XVE Thoratec PulsatileFDA approval for BTT in 2001 and DT in 2003. CE Mark

Authorized. Rarely used anymore due to reliability concerns.

HeartMate II Thoratec Rotor driven continuous axial flow, ball and cup bearings.Approved for use in North America and EU. CE MarkAuthorized. FDA approval for BTT in April 2008. Recently

approved by FDA in the US for Destination Therapy (as at

January 2010).

HeartMate III Thoratec Continuous flow driven by a magnetically suspended axial flow rotor. Pivotal trials for HeartMate III expected 2013.

Incor Berlin Heart Continuous flow driven by a magnetically suspended axial flow rotor.Approved for use in European Union. Used on humanitarian

approvals on case by case basis in the US. Entered clinical

trials in the US in 2009.

Excor Pediatric Berlin Heart External membrane pump device designed for children.Approved for use in European Union. FDA granted

Humanitarian Device Exemption for US in December 2011.

Jarvik 2000 Jarvik Heart Continuous flow, axial rotor supported by ceramic bearings.

Currently used in the United States as a bridge to heart

transplant under an FDA-approved clinical investigation. In

Europe, the Jarvik 2000 has earned CE Mark certification for

both bridge-to-transplant and lifetime use. Child version

currently being developed.

MicroMed DeBakey VAD MicroMed Continuous flow driven by axial rotor supported by ceramic bearings.Approved for use in the European Union. The child version is

approved by the FDA for use in children in USA. Undergoing

clinical trials in USA for FDA approval.

VentrAssist VentracorContinuous flow driven by a hydrodynamically suspended centrifugal

rotor.

Approved for use in European Union and Australia. Company

declared bankrupt while clinical trials for FDA approval were

underway in 2009. Company now dissolved and intellectual

property sold to Thoratec.

MTIHeartLVAD MiTiHeart Corporation Continuous flow driven by a magnetically suspended centrifugal rotor. Yet to start clinical trials.

C-Pulse Sunshine Heart Pulsatile, driven by an inflatable cuff around the aorta. Currently in clinical trials in the US and Australia.

HVAD HeartWareMiniature "third generation" device with centrifugal blood path and

hydromagnetically suspended rotor that may be placed in the

pericardial space.

Obtained CE Mark for distribution in Europe, January 2009.

Initiated US BTT trial in October 2008 (completed February

2010) and US DT trial in August 2010 (enrolment completed

May 2012).

MVAD HeartWareHeartWare's MVAD Pump is a development-stage miniature ventricular

assist device, approximately one-third the size of HeartWare's HVAD

pump.

HeartWare Completed GLP Studies (September 2011).

DuraHeart Terumo Magnetically levitated centrifugal pump. CE approved, US FDA trials underway as at January 2010.

Thoratec PVAD (Paracorporeal

Ventricular Assist Device)Thoratec

Pulsatile system includes three major components: Blood pump,

cannulae and pneumatic driver (dual drive console or portable VAD

driver).

CE Mark Authorized. Received FDA approval for BTT in 1995

and for post-cardiotomy recovery (open heart surgery) in

1998.

IVAD Implantable Ventricular Assist

Device Thoratec

Pulsatile system includes three major components: Blood pump,

cannulae and pneumatic driver (dual drive console or portable VADdriver).

CE Mark Authorized. Received FDA approval for BTT in 2004.

Authorized only for internal implant, not for paracorporealimplant due to reliability issues.
http://www.worldheart.com/index.cfmhttp://www.thoratec.com/http://www.thoratec.com/http://www.berlinheart.de/index.php/mp/content/products/incorhttp://www.berlinheart.de/http://www.berlinheart.de/index.php/mp/content/products/excor_pediatrichttp://www.jarvikheart.com/basic.asp?id=19http://www.jarvikheart.com/http://www.micromedcv.com/productprofile.htmhttp://www.micromedcv.com/http://en.wikipedia.org/wiki/MiTiHeart_Corporationhttp://www.sunshineheart.com/C-Pulsehttp://www.sunshineheart.com/http://www.heartware.com.au/IRM/content/usa/products_HVAD.htmlhttp://www.heartware.com.au/http://www.heartware.com.au/irm/content/products_MVAD.htmlhttp://www.terumoheart.com/http://en.wikipedia.org/wiki/Terumohttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-pvad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-pvad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-ivad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-pvad.aspxhttp://www.thoratec.com/medical-professionals/vad-product-information/thoratec-pvad.aspxhttp://en.wikipedia.org/wiki/Terumohttp://www.terumoheart.com/http://www.heartware.com.au/irm/content/products_MVAD.htmlhttp://www.heartware.com.au/http://www.heartware.com.au/IRM/content/usa/products_HVAD.htmlhttp://www.sunshineheart.com/http://www.sunshineheart.com/C-Pulsehttp://www.sunshineheart.com/C-Pulsehttp://www.sunshineheart.com/C-Pulsehttp://en.wikipedia.org/wiki/MiTiHeart_Corporationhttp://en.wikipedia.org/wiki/MiTiHeart_Corporationhttp://en.wikipedia.org/wiki/MiTiHeart_Corporationhttp://www.micromedcv.com/http://www.micromedcv.com/productprofile.htmhttp://www.jarvikheart.com/http://www.jarvikheart.com/basic.asp?id=19http://www.jarvikheart.com/basic.asp?id=19http://www.jarvikheart.com/basic.asp?id=19http://www.berlinheart.de/index.php/mp/content/products/excor_pediatrichttp://www.berlinheart.de/http://www.berlinheart.de/index.php/mp/content/products/incorhttp://www.thoratec.com/http://www.thoratec.com/http://www.worldheart.com/index.cfm


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Right Ventricular Assist Device

The RVAD assists isolated right ventricular dysfunction by pumping bloodfrom right atrium to pulmonary artery


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Placement Surgically placed Drainage cannula from left (right) atrium and outflow cannula

to ascending aorta (pulmonary a., descending aorta)

Drainage is dependent on pressure gradient, gravity.

Flow rate used depends on the indication for the pump, and is

gradually decreased as the patient is weaned from the pump.

Flow rates in general are 3-5L/min


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Thoratec VAD Right, left or biventricular assist.

Most commonly used as a bridge to transplantation; hasalso been used for post-cardiotomy cardiogenic shock.

Non-portable, however patients can ambulate (unlike

centrifugal pumps). Inpatient use only. Pneumatic drive unit can be synchronized to the patients

ECG or run at a fixed rate.

Pulsatile pump consists of a smooth polyurethane inner sac

in a rigid case. Lays on abdomenal wall. 65cc SV, 6.5L/min max flow rate.

Very expensive!


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Biventricular Assist Device

Thoratec. BIVAD


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Heartmate

Pneumatically or electrically driven pulsatile pump.

For use as a bridge to transplant only.

Implanted in the LUQ with the drive line exiting the LLQ.

Electrical version can be connected to a portable battery.

Max SV 85cc and max flow rate of 12L/M.

Internal sensor measures filling volume and pump output.

Pusher plate covered with sintered polyurethane and

housing surface sintered titanium therefore anticoagulation

not necessary.


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HeartMate XVE LVAS

Portable controllerallows for homedischarge

Does not requireanticoagulation

Percutaneous exit site

BSA > 1.5 m2


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HeartMate II LVAD

Small continuous flowLVAD

Single moving part

Allows excellentfunction/activity

Designed to providesupport for 5-10 yrs

Controller Batteries


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Novocor

For use as bridge to transplantation only.

Implanted in abdomen similar to Heartmate.

Electronically powered pulsatile pusher plate pump.

Has portable battery.

Inner surface is smooth polyurethane.

Max SV 70cc, max flow rate 10L/M.

Anticoagulation with coumadin.


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Berlin Heart VAD

Berlin Heart VAD is a paracorporeal air-driven pulsatile VAD


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Jarvik 2000 System

Javik 2000 is an intraventricular axial flow impeller pump requiringpercutaneous electric power of possible implanted battery power


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Complications with VADs Uncontrolled hemorrhage (most common early comp)

Thrombosis and emboli (CVA)

MOFS (encephalopathy, ARDS, ARF, etc.)

Infection

Failure to maintain pump flow.

*RV failure

*volume

*drainage cannula obstruction

*pulmonary HTN


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BVAD vs TAH BVADs are heterotopic pump which assist the working

ventrical.

TAH are orthotopic pumps which take the place of the heart

both physiologically and anatomically. Single pump.

Surgery Dor technique


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Su ge y o tec que

Extracorporeal Membrane


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Extracorporeal Membrane

Oxygenation (ECMO)Advantages & disadvantages

Possibility of providing total cardiopulmonarysupport and allowing for cardiac and pulmonaryhealing, but needs for higher level of

anticoagulation, leads to bleeding, increased bloodloss, blood product requirement, multipleexploration, and potential infection

IndicationsNeonatal respiratory failurePediatric respiratory failureNeonatal and pediatric cardiac failureAdult cardiorespiratory failure


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Extracorporeal Membrane Oxygenation

Provides both oxygenation and circulation of blood

Unlike cardiopulmonary bypass, whose duration of use ismeasured in hours, ECMO can be used for 3-10 days

One cannula is placed percutaneously via the right jugularvein or femoral vein into the right atrium, or it is placedsurgically into the right atrial appendage, and anothercannula is placed arterially either in the femoral artery orin the aortic arch

The drained venous blood is pumped through the ECMOdevice, where it is oxygenated, warmed, andanticoagulated. It is then returned to the arterialcirculation


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Extracorporeal Membrane Oxygenation

Heart transplantNot included:

1) Low LVEF2) History of NYHA class III/IV heart failure


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Heart transplant

Absolute indications Relative indications

Refractory cardiogenic shock

Dependence on IV inotropicsupport for adequacy of organ

perfusion Peak oxygen consumption per unit

time (VO2) less than 10 mL/kg/min

Severe ischemic symptoms withconsistent limitations of routineactivity that are not amenable to

revascularization procedures(CABG, percutaneous coronaryintervention)

Recurrent symptomatic ventriculararrhythmias despite all therapeutic

interventions

Peak VO2 between 11 and 14mL/kg/min (or 55% ofpredicted) with major

limitation of routineactivities

Recurrent unstable ischemiathat is not amenable to othertreatment

Recurrent instability of f luidbalance/renal functiondespite patient compliance

with medical therapy

symptoms3) Peak VO2 >15 mL/kg/min (and >55%predicted)

Contraindications


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Current alcohol and/or drug abuse

Lack of compliance Uncontrolled or mental health disease

Active malignancy

Multiorgan systemic disease

Active infection except for LVAD infection Significant renal failure (creatinine clearance < 50 mL/min),

significant hepatic dysfunction, or pulmonary disease (FEV1 15 mmHg)

Recent thromboembolic complications

Unhealed peptic ulcer

Other serious comorbidity with a poor prognosis


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Total Artificial Heart (TAH)


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Total Artificial Heart (TAH) In 1969, Dr. Denton Cooley implanted the Liotta TAH

(which is no longer made) TAH has several potential advantages, including the ability

to assist patients with severe biventricular failure; a lack ofdevice pocket and thus a lessened risk of infection; and the

opportunity to treat patients with systemic diseases (eg,amyloidosis, malignancy) who are not otherwisecandidates for transplantation

At present, 2 TAHs are receiving the most attention:

- SynCardia TAH (SynCardia Systems, Inc)

- AbioCor TAH (Abiomed, Inc)


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SynCardia The SynCardia TAH is a structural cousin of the

original Jarvik-7 TAH (Jarvik Heart, Inc) that wasimplanted into patient Barney Clark with great

publicity in 1982. In 2004, investigators reported data that allowed this

device to receive FDA approval for use as a bridge totransplantation.

AbioCor


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AbioCor The AbioCor TAH involves a novel method of

transcutaneous transmission of energy, freeing the patientfrom external drivelines.

The patient exchanges the external battery packs, whichcan last as long as 4 hours.

This TAH is unique in that it is the first TAH to use coils totransmit power across the skin; therefore, notranscutaneous conduits are needed.

This feature allows for the advantages of a closed system,which potentially reduces sources of infection, a knowncomplication of earlier devices.

A limitation of the AbioCor TAH is its large size


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AbioCor Carmat

St

Definition of Stage Usual Therapies


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Stage

Stage A Those at high risk for developing heart failure.

Includes people with:

Hypertension

Diabetes mellitus

Coronary artery disease (including heart attack)

History of cardiotoxic drug therapy

History of alcohol abuse

History of rheumatic fever

Family history of cardiomyopathy.

Exercise regularly

Quit smoking

Treat hypertension

Treat lipid disorders

Discourage alcohol or illicit drug use

If previous heart attack or current diabetes mellitus or hypertension

angiotensin converting enzyme inhibitor (ACE-I)

Stage B Those diagnosed with systolic heart failure but

have never had symptoms of heart failure

(usually by finding an ejection fraction of less than

40% on echocardiogram).

Care measures in Stage A +

All patients should be on ACE-I

Beta-blockers should be addedSurgical consultation for coronary artery revascularization and valve

repair/replacement (as appropriate)

Stage C Patients with known heart failure with current or

priorsymptoms.

Symptoms include:

Shortness of breath

Fatigue

Reduced exercise intolerance.

In this group, care measures from Stage A apply, ACE-I and beta-

blockers should be used +

Diuretics (water pills)

Digoxin

Dietary sodium (salt) restriction

Weight monitoring

Fluid restriction (as appropriate)Withdrawal of drugs that worsen the condition

Spironolactone when symptoms remain severe with other therapies

Stage D Presence of advanced symptoms, afterassuring

optimized medical care

All therapies under Stages A, B and C + evaluation for:

Cardiac transplantation

Ventricular assist devices

Surgical options

Research therapies

Continuous intravenous inotropic infusions

End-of-life care

Young and healthy hearts


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Young and healthy hearts

Documents

Insuficienta cardiaca1