Transcript Heart Failure

Heart Failure
J.B. Handler, M.D.
Physician Assistant Program
University of New England
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Abbreviations
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CO- cardiac output
PCW- pulmonary capillary wedge
SVR- systemic vascular resistance
SVR  PVR (peripheral vascular
resistance)
HR- heart rate
JVD- jugular venous distension
A+V- arterial and venous
C- cardiac
EF- ejection fraction
ED- emergency department
LHF- left heart failure
BVF- biventricular failure
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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
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Heart Failure: Definition
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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.
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Heart Failure Basics
Over 5 million patients in U.S. with HF
 550,000 patients newly diagnosed each year
 > 1 million hospitalizations/yr- HF as 1st Dx; >2.5
hospitalizations- HF among Dx.
  number of HF deaths in spite of advances in Rx:
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– Increased salvage of patients with acute MI
– Numbers are rising as “baby boomers” age
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Management must be individualized
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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
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Precipating Causes
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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
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HF: Systolic or Diastolic?
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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.
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HF: Acute or Chronic?
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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.
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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!
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Cardiac Pressures
4-12
4-12
4-12
8-15
4-12
4-12
4-12
Images.google.com
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-angiotensinaldosterone system.
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Compensatory Mechanisms
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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.
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Adrenergic Nervous System
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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
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Renin-Angiotensin System
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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.
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Renin-Angiotensin System
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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).
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Functional Classification of Heart
Disease: NYHA Criterion
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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.
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Clinical Manifestation of HF
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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
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Fatigue, weakness, abdominal symptoms,
decreased exercise capacity; reflects CO to
muscles, GI tract and other organs.
Cerebral symptoms (esp. in patients with coexisting 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 >20 
interstitial edema; PCW > 25  alveolar edema.
A medical emergency usually addressed in ED.
*PCW: Pulmonary Capillary Wedge pressure
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Physical Exam (L+R sided HF)
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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.
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Physical Exam (L+R sided HF)
Increased systemic venous pressure; JVD reflects
JVP.
 + Hepato-Jugular Reflux.
 Congestive hepatomegaly- enlarged, tender,
pulsatile liver.
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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.
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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.
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CxR: CHF
-type Natriuretic Peptide
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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 (a&v) and diuretic properties- new Rx
for treating refractory heart failure (below).
Normal is < 100 pg/ml
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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
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– ACE inhibitors, Angiotensin Receptor
blockers and others.
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Pathophysiologic Basis of Therapy
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Myocardial systolic failure -Rx. to improve
contractility- Digoxin; sympathomimetics.
Slow progression of cardiac deteriorationACE inhibitors
Beta blockers
Prevent Remodeling
Spironolactone
Improve diastolic dysfunction if possible:
regression of LVH with treatment of co-existing
HTN
Treat arrhythmias as needed
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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.
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HF: Goals of Therapy
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Removal of precipitating factors.
Treatment of underlying cause active ischemia,
valvular disease, cardiomyopathy, etc.
Control of the HF state:
Reduction of cardiac workload
Control of excessive Na/water retention
Enhancement of cardiac contractility
Early initiation of ACEI therapy for most patients
– Hydralazine and nitrates in black populations; added to ACEI
if needed.
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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).
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– No added salt; no salt in preparation of foods; avoid
foods with high sodium content.
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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 CHFFurosemide, Bumetanide, Torsemide
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– Metolazone - similar to thiazide diuretics;
added to and potentiate loop diuretics in severe,
refractory heart failure; caution K
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Diuretics
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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
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Vasodilator Therapy in HF
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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.
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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
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ACE Inhibitors
Superior to all other treatment of HF in terms
of long-term symptomatic improvement and
outcome - Reduce mortality by >25+%.
 Long term ACEI has significant natriuretic effects
resulting in improved diuresis.
 Captopril, enalapril, lisinopril, ramipril,
fosinopril, perindopril et al; all equally beneficial.
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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.
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LV Remodeling
NYerRN
Limitations of ACEI
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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
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Must monitor renal function; Cr and BUN often increase
mildly (and expectedly) with ACEI.
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Angiotensin II Receptor Blockers
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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.
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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.
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Beta-Blocker Therapy
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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.
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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.
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Actions of Spironolactone
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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.
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Aldosterone Blockade Post MI
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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.
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Adjunct Rx to ACEI. Should be considered early in Rx
of patients with large MI/LV dysfunction and heart
failure.
Must monitor K closely
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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.
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Digoxin
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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 (PVC’s, atrial tachycardia) and
2nd/3rd degree A-V block.
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Sympathomimmetic Amines
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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 receptors
High dose- Stimulates Alpha receptors.
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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.
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Nesiritide
New- recombinant form of beta natriuretic peptide
(BNP). Indication: refractory HF.
 Potent vasodilator (venous>arteriolar); 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.
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Biventricular Pacing and ICD’s
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Abnormal IVCD results in dyssynchronous contraction.
If QRS > 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
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CRT-D’s address resynchronization pacing + ICD
*CRT: cardiac resynchronization therapy
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End-Stage Heart Failure
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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.
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Cardiac Transplantation
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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
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Acute Pulmonary Edema
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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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