Upload
ioana-bojescu-rou
View
241
Download
0
Embed Size (px)
Citation preview
8/13/2019 Insuficienta cardiaca1
1/118
8/13/2019 Insuficienta cardiaca1
2/118
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
8/13/2019 Insuficienta cardiaca1
3/118
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
8/13/2019 Insuficienta cardiaca1
4/118
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
8/13/2019 Insuficienta cardiaca1
5/118
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).
8/13/2019 Insuficienta cardiaca1
6/118
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)
8/13/2019 Insuficienta cardiaca1
7/118
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.
8/13/2019 Insuficienta cardiaca1
8/118
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.
8/13/2019 Insuficienta cardiaca1
9/118
Controversial Definitions
8/13/2019 Insuficienta cardiaca1
10/118
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.
8/13/2019 Insuficienta cardiaca1
11/118
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
8/13/2019 Insuficienta cardiaca1
12/118
Underlying causes - 2
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
8/13/2019 Insuficienta cardiaca1
13/118
Underlying causes - 3
Right heart failure
Left ventricular failure
Coronary artery disease (ischemia) Pulmonary hypertension
Pulmonary valve stenosis
Pulmonary embolism
Chronic pulmonary disease Neuromuscular disease
8/13/2019 Insuficienta cardiaca1
14/118
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
8/13/2019 Insuficienta cardiaca1
15/118
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
8/13/2019 Insuficienta cardiaca1
16/118
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.
8/13/2019 Insuficienta cardiaca1
17/118
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.
8/13/2019 Insuficienta cardiaca1
18/118
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).
8/13/2019 Insuficienta cardiaca1
19/118
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
8/13/2019 Insuficienta cardiaca1
20/118
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
8/13/2019 Insuficienta cardiaca1
21/118
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.
8/13/2019 Insuficienta cardiaca1
22/118
8/13/2019 Insuficienta cardiaca1
23/118
Cardiovascular Medical History Hx of heart failure
Angina
MI
CABG
PCI
Pacemaker/ICD
Embolic events
arrhythmias
CVA
PVD
Rheumatic Dx
Other valvular hx
Congenital
8/13/2019 Insuficienta cardiaca1
24/118
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
8/13/2019 Insuficienta cardiaca1
25/118
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.
8/13/2019 Insuficienta cardiaca1
26/118
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
8/13/2019 Insuficienta cardiaca1
27/118
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.
8/13/2019 Insuficienta cardiaca1
28/118
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
8/13/2019 Insuficienta cardiaca1
29/118
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
8/13/2019 Insuficienta cardiaca1
30/118
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
8/13/2019 Insuficienta cardiaca1
31/118
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
8/13/2019 Insuficienta cardiaca1
32/118
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
8/13/2019 Insuficienta cardiaca1
33/118
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
8/13/2019 Insuficienta cardiaca1
34/118
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
8/13/2019 Insuficienta cardiaca1
35/118
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
8/13/2019 Insuficienta cardiaca1
36/118
Staging of Heart Failure
8/13/2019 Insuficienta cardiaca1
37/118
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
8/13/2019 Insuficienta cardiaca1
38/118
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
8/13/2019 Insuficienta cardiaca1
39/118
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
8/13/2019 Insuficienta cardiaca1
40/118
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)
8/13/2019 Insuficienta cardiaca1
41/118
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
8/13/2019 Insuficienta cardiaca1
42/118
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)
8/13/2019 Insuficienta cardiaca1
43/118
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
8/13/2019 Insuficienta cardiaca1
44/118
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
8/13/2019 Insuficienta cardiaca1
45/118
Non-pharmacologic therapy
8/13/2019 Insuficienta cardiaca1
46/118
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
8/13/2019 Insuficienta cardiaca1
47/118
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
8/13/2019 Insuficienta cardiaca1
48/118
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
8/13/2019 Insuficienta cardiaca1
49/118
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.
8/13/2019 Insuficienta cardiaca1
50/118
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.
8/13/2019 Insuficienta cardiaca1
51/118
Role of RAS in HF
8/13/2019 Insuficienta cardiaca1
52/118
Role of ACE-I
8/13/2019 Insuficienta cardiaca1
53/118
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
8/13/2019 Insuficienta cardiaca1
54/118
8/13/2019 Insuficienta cardiaca1
55/118
8/13/2019 Insuficienta cardiaca1
56/118
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.
8/13/2019 Insuficienta cardiaca1
57/118
Tolvaptan
8/13/2019 Insuficienta cardiaca1
58/118
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.htm8/13/2019 Insuficienta cardiaca1
59/118
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
8/13/2019 Insuficienta cardiaca1
60/118
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)
8/13/2019 Insuficienta cardiaca1
61/118
8/13/2019 Insuficienta cardiaca1
62/118
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
8/13/2019 Insuficienta cardiaca1
63/118
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.
8/13/2019 Insuficienta cardiaca1
64/118
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
8/13/2019 Insuficienta cardiaca1
65/118
8/13/2019 Insuficienta cardiaca1
66/118
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
8/13/2019 Insuficienta cardiaca1
67/118
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.
8/13/2019 Insuficienta cardiaca1
68/118
8/13/2019 Insuficienta cardiaca1
69/118
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
8/13/2019 Insuficienta cardiaca1
70/118
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.
8/13/2019 Insuficienta cardiaca1
71/118
Example of one VADdevice:HeartMate Implantable
h VA i f
8/13/2019 Insuficienta cardiaca1
72/118
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
8/13/2019 Insuficienta cardiaca1
73/118
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
8/13/2019 Insuficienta cardiaca1
74/118
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
8/13/2019 Insuficienta cardiaca1
75/118
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.
8/13/2019 Insuficienta cardiaca1
76/118
8/13/2019 Insuficienta cardiaca1
77/118
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.
8/13/2019 Insuficienta cardiaca1
78/118
Ideal requirements1. Durable2. Biocompatible
3. Nonthrombogenic4. Resistant to infection
5. Reasonably priced
6. Available numerous size
8/13/2019 Insuficienta cardiaca1
79/118
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
8/13/2019 Insuficienta cardiaca1
80/118
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
8/13/2019 Insuficienta cardiaca1
81/118
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.cfm8/13/2019 Insuficienta cardiaca1
82/118
8/13/2019 Insuficienta cardiaca1
83/118
Right Ventricular Assist Device
The RVAD assists isolated right ventricular dysfunction by pumping bloodfrom right atrium to pulmonary artery
8/13/2019 Insuficienta cardiaca1
84/118
8/13/2019 Insuficienta cardiaca1
85/118
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
8/13/2019 Insuficienta cardiaca1
86/118
8/13/2019 Insuficienta cardiaca1
87/118
8/13/2019 Insuficienta cardiaca1
88/118
8/13/2019 Insuficienta cardiaca1
89/118
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!
8/13/2019 Insuficienta cardiaca1
90/118
Biventricular Assist Device
Thoratec. BIVAD
8/13/2019 Insuficienta cardiaca1
91/118
8/13/2019 Insuficienta cardiaca1
92/118
8/13/2019 Insuficienta cardiaca1
93/118
8/13/2019 Insuficienta cardiaca1
94/118
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.
8/13/2019 Insuficienta cardiaca1
95/118
HeartMate XVE LVAS
Portable controllerallows for homedischarge
Does not requireanticoagulation
Percutaneous exit site
BSA > 1.5 m2
8/13/2019 Insuficienta cardiaca1
96/118
HeartMate II LVAD
Small continuous flowLVAD
Single moving part
Allows excellentfunction/activity
Designed to providesupport for 5-10 yrs
Controller Batteries
8/13/2019 Insuficienta cardiaca1
97/118
8/13/2019 Insuficienta cardiaca1
98/118
8/13/2019 Insuficienta cardiaca1
99/118
8/13/2019 Insuficienta cardiaca1
100/118
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.
8/13/2019 Insuficienta cardiaca1
101/118
8/13/2019 Insuficienta cardiaca1
102/118
Berlin Heart VAD
Berlin Heart VAD is a paracorporeal air-driven pulsatile VAD
8/13/2019 Insuficienta cardiaca1
103/118
Jarvik 2000 System
Javik 2000 is an intraventricular axial flow impeller pump requiringpercutaneous electric power of possible implanted battery power
8/13/2019 Insuficienta cardiaca1
104/118
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
8/13/2019 Insuficienta cardiaca1
105/118
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
8/13/2019 Insuficienta cardiaca1
106/118
Su ge y o tec que
Extracorporeal Membrane
8/13/2019 Insuficienta cardiaca1
107/118
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
8/13/2019 Insuficienta cardiaca1
108/118
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
8/13/2019 Insuficienta cardiaca1
109/118
Extracorporeal Membrane Oxygenation
Heart transplantNot included:
1) Low LVEF2) History of NYHA class III/IV heart failure
8/13/2019 Insuficienta cardiaca1
110/118
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
8/13/2019 Insuficienta cardiaca1
111/118
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
8/13/2019 Insuficienta cardiaca1
112/118
Total Artificial Heart (TAH)
8/13/2019 Insuficienta cardiaca1
113/118
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)
8/13/2019 Insuficienta cardiaca1
114/118
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
8/13/2019 Insuficienta cardiaca1
115/118
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
8/13/2019 Insuficienta cardiaca1
116/118
AbioCor Carmat
St
Definition of Stage Usual Therapies
8/13/2019 Insuficienta cardiaca1
117/118
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
8/13/2019 Insuficienta cardiaca1
118/118
Young and healthy hearts