Heart Failure - PowerPoint PPT Presentation

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Heart Failure

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Heart Failure J.B. Handler, M.D. Physician Assistant Program University of New England * – PowerPoint PPT presentation

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Title: Heart Failure


1
Heart Failure
  • J.B. Handler, M.D.
  • Physician Assistant Program
  • University of New England

2
Abbreviations
  • CO- cardiac output
  • PCW- pulmonary capillary wedge
  • SVR- systemic vascular resistance
  • SVR ? PVR (peripheral vascular resistance)
  • HR- heart rate
  • JVD- jugular venous distension
  • AV- arterial and venous
  • C- cardiac
  • EF- ejection fraction
  • ED- emergency department
  • LHF- left heart failure
  • BVF- biventricular failure
  • P- Pulmonary
  • ACEI- angiotensin converting enzyme inhibitor
  • ARB- angiotensin receptor blocker
  • NYHA- New York Heart Association criterion
  • BNP- beta natiuretic peptide
  • MVO2- myocardial oxygen consumption
  • ICD- implantable cardioverter defibrillator
  • RHF- right heart failure
  • CRT- cardiac resynchronization therapy

3
Heart Failure Definition
  • A pathophysiologic state in which an abnormality
    of cardiac function is responsible for failure of
    the heart to pump blood at a rate commensurate
    with the requirements of the metabolizing tissues
    and/or can do so only from an abnormally elevated
    diastolic volume/pressure.

4
Heart Failure Basics
  • Over 5 million patients in U.S. with HF
  • 550,000 patients newly diagnosed each year
  • gt 1 million hospitalizations/yr- HF as 1st Dx
    gt2.5 hospitalizations- HF among Dx.
  • ? number of HF deaths in spite of advances in Rx
  • Increased salvage of patients with acute MI
  • Numbers are rising as baby boomers age
  • Management must be individualized

5
Etiologies of Heart Failure (HF)
  • Coronary Heart Disease MI(s) or ischemia
    superimposed on prior infarction(s)? 75 of all
    cases.
  • Primary pump failure - Cardiomyopathy, viral
    myocarditis
  • Valvular heart disease
  • Congenital heart disease
  • Long standing, uncontrolled hypertension

6
Precipating Causes
  • Progressive weakening of the myocardium and
    consequences? heart failure
  • Infection
  • Anemia
  • Thyrotoxicosis
  • Arrhythmias
  • Aggravation of hypertension
  • Myocardial ischemia or infarction
  • Physical, dietary (Na/fluid) or emotional
    excesses

7
HF Systolic or Diastolic?
  • Systolic Failure (or dysfunction) Primary
    contraction abnormality inadequate delivery of
    O2 to tissues and associated symptoms e.g
    large or multiple MI(s), dilated cardiomyopathy,
    chronic AR, MR.
  • Diastolic Failure (or dysfunction) - Impaired
    ventricular relaxation- elevation of ventricular
    filling pressures and associated symptoms e.g
    long standing hypertension (with LVH),
    hypertrophic cardiomyopathy, acute ischemia,
    prior infarcts, restrictive cardiomyopathy.
  • Systolic and diastolic failure often occur
    together.

8
HF Acute or Chronic?
  • Acute - Large MI? sudden onset of symptoms,
    systolic failure, hypotension, pulmonary edema.
  • Chronic - pathophysiology and symptoms develop
    slowly, BP usually maintained until late in
    course peripheral edema common e.g dilated
    cardiomyopathy, chronic valvular insufficiency,
    large or multiple infarcts.
  • Acute episodes may be superimposed on chronic HF?
    development of pulmonary edema in patient with
    previously compensated (treated) HF.

9
HF Rt Sided or Lt Sided?
  • Lt sided failure e.g post MI, aortic/mitral
    valve disease. Inadequate CO with pulmonary
    congestion and related symptoms.
  • Rt. sided failure e.g COPD/pulmonary
    hypertension, pulmonic stenosis associated with
    peripheral edema, hepatic congestion, etc.
  • Most common cause of right sided failure is
    left sided failure/dysfunction!

10
Cardiac Pressures
4-12
4-12
4-12
4-12
4-12
4-12
8-15
Images.google.com
11
HF Backward or Forward?
  • Backward failure Inadequate ventricular
    emptying pressures in the atrium and venous
    system behind the failing ventricle rise
    resulting in transudation of fluid into
    interstitial spaces.
  • Forward failure Inadequate forward CO Na and
    water retention result from diminished renal
    perfusion and activation of renin-angiotensin-aldo
    sterone system.

12
Compensatory Mechanisms
  • Redistribution of CO Blood flow redistributed to
    vital organs- brain and myocardium with reduced
    blood flow to skin and muscle? mediated via
    activation of the adrenergic nervous system and
    vasoconstriction to less vital tissues.
  • Na and water retention Complex sequence of
    adjustments occurs resulting in accumulation of
    fluid and increasing SVR
  • Helps maintain CO via Starling mechanism
  • Cost is volume overload and ?afterload.

13
Adrenergic Nervous System
  • Activated in CHF-beneficial and harmful.
  • Increase levels of norepinephrine result in
    increase HR, contractility and SVR- helps
    maintain arterial perfusion pressure (BP) in
    presence of decreased CO.
  • Elevation of SVR results in increased hemodynamic
    burden (afterload) and O2 requirement of the
    failing ventricle. Long term elevation of
    catecholamines lead to progressive myocardial
    damage and fibrosis.

BP CO x SVR
CO BP/SVR
14
Renin-Angiotensin System
  • Renin enzyme released by kidneys if ?perfusion
    or ?BP.
  • Angiotensinogen (renin substrate) converted to
    Angiotensin I by renin.
  • Angiotensin I converted to Angiotensin II in
    lungs by angiotensin converting enzyme.
  • Angiotensin II extremely potent
    vasoconstrictor- leads to arteriolar constriction
    and increase in SVR, raising BP.

15
Renin-Angiotensin System
  • Angiotensin II stimulates adrenal gland to
    secrete Aldosterone.
  • Aldosterone a mineralocorticoid hormone increases
    renal Na and H2O reabsorption.
  • Renin-angiotensin-aldosterone activation (by
    decreased cardiac output) in heart failure is a
    major factor in edema formation and increased
    SVR.
  • Long term activation of angiotensin II and
    aldosterone lead to myocardial thinning and
    fibrosis (remodeling).

16
Functional Classification of Heart Disease NYHA
Criterion
  • I No limitation of physical activity. No
    symptoms of SOB, CP dizzyness, etc.
  • II Slight limitation of physical activity. Some
    (ordinary) activities (exercise, exertion, etc)
    cause symptoms.
  • III Marked limitation of physical activity. Less
    than ordinary activities (walking, dressing,
    etc.) cause symptoms.
  • IV Symptomatic at rest or minimal activity
    unable to engage in any physical activity.

17
Clinical Manifestation of HF
  • Dyspnea Initially with activity, then at rest
    due to elevation of pulmonary venous pressure.
  • Orthopnea Dyspnea in recumbent position
    redistribution of fluid from abdomen and lower
    extremities into chest.
  • Paroxysmal Nocturnal Dyspnea Attacks of severe
    SOB, coughing and wheezing awakening patient from
    sleep.
  • Unexplained weight gain Sodium and water
    retention. Patients may note swelling of the
    legs.
  • Nocturia commonly occurs

18
  • Fatigue, weakness, abdominal symptoms, decreased
    exercise capacity reflects ?CO to muscles, GI
    tract and other organs.
  • Cerebral symptoms (esp. in patients with
    co-existing cerebrovascular disease) Decreased
    perfusion to brain.
  • Acute Pulmonary Edema Severe dyspnea at rest as
    pulmonary congestion progresses accompanied by
    marked elevation of pulmonary capillary pressure
    leading to alveolar edema PCW gt20 ?
    interstitial edema PCW gt 25 ? alveolar edema. A
    medical emergency usually addressed in ED.

PCW Pulmonary Capillary Wedge pressure
19
Physical Exam (LR sided HF)
  • Symptoms vary depending on severity.
  • Patient may be uncomfortable lying flat BP
    normal or low tachycardia common. Cyanosis of
    lips nailbeds reflects hypoxemia.
  • Crackles (Rales- older term)- moist inspiratory
    crackles wheezes. Begin at bases and progress
    upwards through the lungs.
  • S3 gallop- low pitched sound in early diastole.

20
Physical Exam (LR sided HF)
  • Increased systemic venous pressure JVD reflects
    ?JVP.
  • Hepato-Jugular Reflux.
  • Congestive hepatomegaly- enlarged, tender,
    pulsatile liver.

21

Physical Exam
  • Peripheral edema develops with progressive HF.
  • Hydrothorax and ascites- pleural effusions.
  • Cardiac cachexia- Wasted appearance occurs with
    severe chronic heart failure?weight loss,
    anorexia, nausea correlates with increased
    levels of cytokines like circulating tumor
    necrosis factor.

22
Additional Findings
  • CxR Cardiomegaly distension of pulmonary veins
    venous redistribution to apices
    interstitial?alveolar edema pleural effusions.
  • Echo-Doppler- findings unique to pathology
    responsible for HF best non-invasive tool.
    Identifies ventricular dysfunction and EF.
  • ECG- may reflect underlying pathology i.e.
    infarct, LVH, arrhythmia, etc.

23

CxR CHF
24
?-type Natriuretic Peptide
  • ?NP- hormone produced by heart (ventricle) in
    response to wall stress- marker of decompensated
    heart failure in blood.
  • Blood test for acute ventricular dysfunction ?
    symptomatic heart failure
  • Useful in diagnosis of HF in patients presenting
    with SOB of uncertain (C vs P) etiology and
    confirming HF when suspected clinically.
  • Has vasodilator (av) and diuretic properties-
    new Rx for treating refractory heart failure
    (below).
  • Normal is lt 100 pg/ml

25
Pathophysiologic Basis of Therapy
  • Taylor treatment to the manifestations of heart
    failure in each individual patient.
  • Excessive increase in preload diuretics,
    venodilators (nitrates).
  • Excess Na retention with edema diuretics.
  • Increased afterload Vasodilator therapy
  • ACE inhibitors, Angiotensin Receptor blockers
    and others.

26

Pathophysiologic Basis of Therapy
  • Myocardial systolic failure -Rx. to improve
    contractility- Digoxin sympathomimetics.
  • Slow progression of cardiac deterioration- ACE
    inhibitorsBeta blockers Spironolactone
  • Improve diastolic dysfunction if possible
    regression of LVH with treatment of co-existing
    HTN
  • Treat arrhythmias as needed

Prevent Remodeling
27
Mortality in Heart Failure
  • Overall poor prognosis once symptomatic
  • Severe failure (class IV)- 40-50 mortality in 12
    months
  • Moderate failure (class III)- 40-50 mortality in
    3-4 yrs
  • Ejection Fraction (EF) is predictive
  • 30-40 die suddenly- arrhythmia.

28
HF Goals of Therapy
  • Removal of precipitating factors.
  • Treatment of underlying cause? active ischemia,
    valvular disease, cardiomyopathy, etc.
  • Control of the HF stateReduction of cardiac
    workloadControl of excessive Na/water
    retentionEnhancement of cardiac contractility
  • Early initiation of ACEI therapy for most
    patients
  • Hydralazine and nitrates in black populations
    added to ACEI if needed.

29
Treatment of HF
  • Reduction of cardiac workload decreased/limited
    activity elastic stockings, anxiolytic therapy
    anticoagulation for prolonged bed rest.
  • Control excessive dietary sodium (4 gram Na diet
    or less).
  • No added salt no salt in preparation of foods
    avoid foods with high sodium content.

30
Diuretics
  • Early addition of diuretics beneficial in
    relieving symptoms (shortness of breath) and
    reducing preload- does not ?mortality.
  • Loop diuretics Most potent diuretics and
    cornerstone of diuretic Rx in CHF- Furosemide,
    Bumetanide, Torsemide
  • Metolazone - similar to thiazide diuretics added
    to and potentiate loop diuretics in severe,
    refractory heart failure caution ?K

31

Diuretics
  • Loop diuretics remain effective in renal failure.
  • Must monitor renal function (BUN, Cr.) serum
    electrolytes (esp. K), uric acid and glucose
    loop diuretics can cause hypokalemia, and
    hyperuricemia as well as metabolic alkalosis.
  • Over aggressive diuresis can lead to pre-renal
    azotemia ?impaired renal fx from hypovolemia and
    ?perfusion.
  • Triamterene and Amiloride are weak diuretics that
    are K sparing - elevate K levels may be used in
    combination with loop diuretics to offset K losses

32
Vasodilator Therapy in HF
  • LV afterload always elevated in HF due to neural
    and humoral influences that act to constrict the
    peripheral vascular bed and elevate SVR preload
    also increased from Na/H20 retention.
  • In presence of impaired cardiac function,
    increasing afterload will reduce cardiac output
    further and lead to elevation of pulmonary
    pressures and pulmonary congestion.
  • In patients with acute and chronic HF, treatment
    with vasodilators results in decreasing SVR,
    increasing CO, decreasing PCW, and relief of
    symptoms also decreases mortality.

33
Angiotensin Converting Enzyme Inhibitors
  • Activation of the Renin-Angiotensin-Aldosterone
    system in heart failure results in marked
    vasoconstriction via Angiotensin II and Na and
    H2O retention via Aldosterone.
  • ACE Inhibitors dramatically reduce afterload, and
    to a lesser degree, preload in patients with HF
    by ?ing the production of Angiotensin II and
    aldosterone.
  • CO BP/SVR

34
ACE Inhibitors
  • Superior to all other treatment of HF in terms of
    long-term symptomatic improvement and outcome -
    Reduce mortality by gt25.
  • Long term ACEI has significant natriuretic
    effects resulting in improved diuresis.
  • Captopril, enalapril, lisinopril, ramipril,
    fosinopril, perindopril et al all equally
    beneficial.

35
ACE Inhibitors
  • ACEI decrease remodeling of the LV post MI and in
    HF by reducing wall thinning, fibrosis and
    interfering with programmed cell death
    (apoptosis) result is ? mortality.
  • Elevation of kinins from ACE inhibition may also
    have beneficial effects on hemodynamics
    (vasodilation) and remodeling increased levels
    of prostaglandins and nitric oxide vasodilation.

36
LV Remodeling
NYerRN
37
Limitations of ACEI
  • Fall in systemic BP. ACEI usually well tolerated
    if initiate with low dose and gradually increase.
  • Cough- Drug related persistent cough resulting
    from elevated bradykinin levels occurs in up to
    15-20 of patients, but only 5 need to DC the
    drug.
  • Less effective in black populations. Hydralazine
    long acting nitrates are added to ACEI prn.
  • BiDil Hydralazine isosorbide dinitrate
  • Must monitor renal function Cr and BUN often
    increase mildly (and expectedly) with ACEI.

38
Angiotensin II Receptor Blockers
  • Released and FDA approved for hypertension.
  • Inhibit angiotensin II receptor - reduce SVR, BP
    and afterload.
  • Similar hemodynamic effects to ACEI.
  • Do not increase bradykinen- no cough but less
    protection against remodeling.
  • Useful as an alternative to ACEI (if pt
    intolerant) sometimes added to ACEI for severe
    HF.
  • Comparison studies ARB vs ACEI have demonstrated
    ACEI superiority in most large clinical trials.

39
Beta-Blocker Therapy
  • Previously contraindicated in treating HF.
  • Now proven that ?-blockers are not only useful in
    treating HF, but reduce mortality as well as
    improve cardiac function and symptoms.
  • Multiple clinical trials using carvedilol,
    metoprolol and bisoprolol (MERIT et al).
  • Begin once patient stable and euvolemic for
    chronic heart failure.

40
Beta-Blocker Therapy
  • Likely that chronic elevations of catecholamines
    and sympathetic nervous system activity cause
    progressive myocardial damage, fibrosis and
    dysfunction?abnormal remodeling.
  • Beneficial for all classes of heart failure with
    up to 30 decrease in mortality.
  • Must begin with very low doses and gradually
    increase e.g carvedilol 3.125 mgs b.i.d.
  • Unclear if all ?-blockers are alike for HF.
    Carvedilol may be drug of choice because of its
    combined ? and ? blocking effects.

41
Aldosterone Antagonists
  • Spironolactone Competitive inhibitor of
    aldosterone has mild diuretic properties and
    elevates K (often used in combination with loop
    diuretics which can cause hypokalemia).
  • In low dose (12.5-25 mgs/daily) spironolactone
    has been shown to decrease morbidity and
    mortality in patients with severe heart failure.
  • Has anti-androgenic properties.
  • Must monitor serum K to avoid hyperkalemia.

42
Actions of Spironolactone
  • Aldosterone mediates some of the deleterious
    effects of renin-angiotensin-aldosterone system
    activation, such as myocardial remodeling and
    fibrosis.
  • By blocking aldosterone, spironolactone should be
    considered as a neurohormonal antagonist rather
    than narrowly as a K sparing diuretic.
  • Clinical trials (RALES et al) show 29 reduction
    in mortality in NYHA class III and IV patients.
  • Eplerenone- released in 2003 aldosterone
    antagonist without anti-androgenic properties.

43
Aldosterone Blockade Post MI
  • Spironolactone and eplerenone post MI reduce
    morbidity and mortality in patients with LV
    dysfunction/heart failure.
  • Mineralocorticoid blockade prevents remodeling,
    blocks collagen production, improves EF and
    decreases LV dilatation.
  • Adjunct Rx to ACEI. Should be considered early
    in Rx of patients with large MI/LV dysfunction
    and heart failure.
  • Must monitor K closely

44
Enhancement of Contractility
  • Digitalis Glycosides - Digoxin most commonly
    used only oral inotropic agent available
    improves cardiac contractility.
  • Increases automaticity of cardiac electrical
    tissue - can induce arrhythmias.

45
Digoxin
  • Prolongs refractory period of AV node (vagal tone
    increased) slows rate of Atrial fibrillation and
    flutter.
  • Modest improvement in cardiac function in
    patients with LV dilatation and dysfunction.
  • Falling out of favor for Rx of CHF improves
    symptom but not mortality.
  • Low Therapeutic/Toxic index- toxicity includes N,
    V, arrhythmias (PVCs, atrial tachycardia) and
    2nd/3rd degree A-V block.

46
Sympathomimmetic Amines
  • Indication refractory HF. Must be given (short
    term) by continuous IV infusion in a hospitalized
    setting, preferably with invasive hemodynamic
    monitoring (rt. heart catheter).
  • Dobutamine Potent inotrope- stimulates Beta
    receptors, raises CO.
  • Dopamine Low dose-dilates renal and mesenteric
    blood vessels via Dopaminergic receptors
    Moderate dose- Stimulates B receptorsHigh dose-
    Stimulates Alpha receptors.

47
Phosphodiesterase Inhibitors
  • Indication refractory HF. Improve cardiac
    contractility by inhibiting myocardial
    phosphodiesterase.
  • Potent inotropes administered IV for short term
    use.
  • Amrinone, Milrinone.
  • Trials using these and other newer inotropes
    orally for long term use have all demonstrated
    substantial increase in mortality.

48
Nesiritide
  • New- recombinant form of beta natriuretic peptide
    (BNP). Indication refractory HF.
  • Potent vasodilator (venousgtarteriolar) decreases
    LV filling pressures (pre-load) and SVR
    (afterload) improves cardiac output.
  • Must monitor renal function- renal failure
    occurs.
  • Continuous IV infusion following a bolus.
  • May have diuretic effects in some individuals.

49
Biventricular Pacing and ICDs
  • Abnormal IVCD results in dyssynchronous
    contraction.
  • If QRS gt 120ms and severe refractory CHF,
    synchronized biventricular pacing (CRT) improves
    symptoms and quality of life may decrease
    mortality.
  • ICD decrease mortality in patients with LV
    dysfunction and symptoms of HF.
  • Indications for ICD
  • Secondary Rescusitated cardiac arrest/Vfib or
    hemodynamically unstable Vtach
  • Primary EF ? .35 mild to moderate HF symptoms
  • CRT-Ds address resynchronization pacing ICD

CRT cardiac resynchronization therapy
50
End-Stage Heart Failure
  • HF unresponsive to intensive medical Rx.
  • LV assist devices Implantable assist device
    (pump) connected to external power supply.
    Decrease workload of native heart and buy time
    (bridge) to heart transplant.
  • Allow mobility and discharge from hospital to
    await transplant. Heart may improve over time.
  • Complications Bleeding, infections,
    thromboembolism.
  • Very expensive 2-300,000 for up to 3 months.

51
Cardiac Transplantation
  • Widely used. Problem Not enough donor hearts.
  • Living donor heart replaces failing one.
  • Improved immunosuppressive drugs yield 70 or
    greater 5 year survival with excellent quality of
    life.
  • High cost- 200,000 initially
  • Complications
  • Rejection, infections, accelerated CHD in donor
    coronary arteries.
  • Immunospuppressive related cancers

52
Acute Pulmonary Edema
  • Medical emergency
  • Treatment modalities may include
  • Morphine sulfate- reflex withdrawal of
    sympathetic tone decreases anxiety
  • O2
  • IV loop diuretics - promote diuresis and have
    direct venodilator activity.
  • Afterload reduction IV Nitroprusside
  • IV Inotropes -Dobutamine
  • Preload reduction- Nitrates
  • Invasive hemodynamic monitoring improves
    management.
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