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Heart Failure
“Defined as a pathophysiological state in
which an abnormality of cardiac function is
the cause of the heart to pump blood at a
rate that is not able to keep up with the
needs of the body.”
Heart Failure
5 million Americans with heart failure today
6-10% of people older than 65 yo have it
500,000 are diagnosed with HF each year
Reason of at least 20% of all hospitalizations (6.5 million
hospital days each year)
Over past decade, rate of hospitalization has increased
by 159% (550,000 to nearly 900,000 per year)
Symptomatic heart failure has a worse prognosis than
most cancers, with a one-year mortality of almost 45%
Thus, we have a strong incentive to identify, predict, and
treat the factors contributing to hospitalizations
Heart Failure
Heart failure is a clinical syndrome arising
from any structural or functional cardiac
disorder that impairs the ability of the
ventricle to fill with or eject blood.
Because not all patients have volume
overload, “heart failure” is generally
preferred to “congestive heart failure”
Two types of heart failure
– EF<40%, dilated LV, Congestion and
cardiomegaly on CXR, S3
– Assoc with previous MI, HTN, DM, sleep
– EF>40%, LV hypertrophy, Congestion without
cardiomegaly on CXR, S4.
– Assoc with HTN, DM, Obesity, COPD, dialysis
Diastolic Heart Failure
Associated conditions include:
– Restrictive (infiltrative) cardiomyopathy:
– Obstructive and nonobstructive hypertrophic
– Pericardial constriction
– LVH from HTN
Characteristics of Patients with Diastolic Heart Failure and Patients with Systolic Heart
Jessup, M. et al. N Engl J Med 2003;348:2007-2018
Diastolic Failure
Diagnosis often made by clinician who
recognizes the typical signs and
Relatively little evidence to guide care of
patients with this condition
Patients are treated with risk factor
modification, controlling blood pressure,
heart rate, ischemia, and volume
Systolic Heart Failure
Coronary artery disease is the cause in 2/3 of
Other causes include:
Thyroid disease
Valvular disease
No identifiable cause (i.e. idiopathic dilated
Heart Failure as Progressive
Ventricular dysfunction begins with injury
or stress to the myocardium, and
The heart chamber generally dilates,
hypertrophies, and becomes spherical
This increases the hemodynamic stress on
the walls of the heart
Left ventricular remodeling involves mechanical,
neurohormonal, and genetic factors that alter the
ventricular size and function
Patients with HF have elevated levels of
norepinephrine, angiotensin II, aldosterone,
endothelin, vasopressin, and cytokines
Remodeling occurs in several conditions,
including myocardial infarction, cardiomyopathy,
hypertension, valvular heart disease
One sees hypertrophy, myocyte death, and
increased interstitial fibrosis
Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure
(Panel B)
Jessup, M. et al. N Engl J Med 2003;348:2007-2018
Consequences of Remodeling
Mitral Regurgitation
Arrhythmias and Bundle Branch Block
Mitral Regurgitation
As the left ventricle dilates and the heart
becomes globular, the papillary muscles
and mitral leaflets change orientation,
leading to distortion of the papillary
Mitral regurgitation results in volume
overload on an overburdened ventricle,
further causing progression of disease
Another consequence of ischemia, inflammation,
fibrosis, and aging is arrhythmia
SVT, especially a. fib., often marks the onset of
systolic or diastolic heart failure
In patients with HTN or abnormal myocardial
function, elevation in ventricular end-diastolic
volume leads to atrial stretch, which in turn
causes electrical instability
Abnormal myocardial conduction can also lead
to left bundle branch block, which is a predictor
of sudden death
LBBB causes abnormal ventricular activation
and contraction, ventricular dyssynchrony,
delayed opening and closure of the aortic and
mitral valves, and abnormal diastolic function
LBBB can result in reduced ejection fraction,
cardiac output, and arterial pressure, and
paradoxical septal motion, increased LV volume,
and mitral regurgitation
Rate of sudden cardiac death in patients
with heart failure is 6-9 times that in the
general population
Typically will present with symptoms of:
– Dyspnea on exertion
– Orthopnea
– Ankle swelling
– Weight gain
– Sometimes abdominal distension
– Tiredness and weakness
Special Questions to ask
Chest pain or exertional angina – strongly suggests IHD as
Recent flu like illness – consider viral myocarditis
History of longstanding alcohol or HTN – consider alcoholic or
hypertensive cardiomyopathy
History of proteinuria or chronic inflammatory condition,
consider amyloid
Recent blood transfusion or Sx consider volume overload
FHx, along with diabetic “bronzed” pt – consider hereditary
Things that worsen underlying heart failure:
Antiarrhythmics – disopyramide and flecanide
Ca channel blockers – esp. Verapamil
B Blockers
Physical exam – look specifically for evidence
of how bad their HF is and clues to the
underlying cause
Sympathetic overdrive (to compensate for low CO) –
evidenced by sinus tachycardia, diaphoresis, and
peripheral vasoconstriction
Pulsus alternans – alternating strong and weak
peripheral pulses, exact pathophysiology not known.
Manifestations of volume overload
Pleural effusions, alveolar edema – crackles
Peripheral edema
Ascites, hepatomegaly, splenomegaly
Ventricular enlargement – displaced PMI
S3 or S4
Pulmonary hypertension – complaints of chest pain, palpable
pulmonic tap, pulmonary insufficiency.
CBC – R/o anemia as ppt.
Chem 7 – assess BUN/Creat/K
LFT – may rise with hepatic congestion
Fasting glucose – screen for DM
TFT – r/o thyrotoxicosis or hypothyroidism
Fe/TIBC – if hemochromatosis is a risk
BNP -- >100 is 90% sensitive for HF, equally as
predictive as finding cardiomegaly on CXR, or
rales on clinical exam. Cost only $20
Prominent upper lobe vessels
Kerley B lines
Pleural effusions
Bats wing pulmonary edema
EKG and Echo
Look for arrhythmias e.g. A fib, V Tach
Conduction abnormalities – esp. seen in pts with
dilated cardiomyopathy
EF – helps distinguish systolic and diastolic HF
Regional wall motion abnormalities suggesting
Valvular disease
Pulmonary artery pressures.
Framingham Criteria
2 major
1major and
2 minor
NYHA (functional classes)
1 yr mortality
Asymptomatic with ordinary activity
Slight limitation of normal function
Marked limitation of physical activities
Dyspneic at rest
ACC/AHA Stages of heart failure
High risk for heart failure without structural disease, currently
Heart disease with asymptomatic LV dysfunction
Prior or current symptoms of Heart failure
Advanced heart disease and severely symptomatic or
refractory heart failure
“Staging” introduced to get people to realize that there is
an element of preventability in HF and that pts need
screening while asymptomatic in order to prevent
progression (just like cancer screening)
Stages of Heart Failure
Examples of patients in each stage:
– Stage A: patients with HTN, CAD, DM, history of
cardiotoxic drug therapy or alcohol abuse, h/o
rheumatic fever, FHx of cardiomyopathy
– Stage B: LVH or fibrosis, LV dilatation or
hypocontractility, asymptomatic valvular heart
disease, previous MI
– Stage C: dyspnea or fatigue due to LV systolic
dysfunction, asymptomatic pts undergoing tx for prior
sx of HF
– Stage D: pts frequently hospitalized for HF and can
not be safely d/c ed from hospital, pts in hospital
awaiting transplant, pts at home receiving IV
inotropes or LVAD, pts in hospice
How do you manage this
Heart Failure
Large trials have looked at the effects of
ACE inhibitors, angiotensin receptor
antagonists, beta-blockers,
spironolactone, biventricular pacing,
CABG, and the use of multidisciplinary
teams. All have been shown to reduce
rates of hospitalization and improve
functional status.
Stage A Heart Failure
Treat risk factors!
Treatment of hypertension decreases incidence of left
ventricular hypertrophy and cardiovascular mortality and
reduces incidence of heart failure by 30-50%
Use of ACE inhibitors in asymptomatic high-risk patients
with DM or vascular disease reduces rate of death, MI,
and stroke
Use of ARBs (losartan) has delayed the first
hospitalization for heart failure in patients with DM and
Goal of treatment is to prevent remodeling!
Stages B, C, and D Heart Failure
Goals of those with low ejection fraction are to
slow progression of disease and alleviate
Lifestyle modification remains a mainstay, for
Moderate sodium restriction
Weight monitoring
Medication regimen compliance
Moderation of alcohol
Exercise program for selected patients
Stages B, C, and D Heart Failure
ACE inhibitors limit the physiologic consequences of
angiotensin II levels, and decrease degradation of
bradykinin (which promotes vasodilation and natriuresis
in the kidney)
ACE inhibitors after an MI improve survival, rates of
hospitalization, symptoms, cardiac output and promote
reverse remodeling
Optimal target dose of ACE inhibitors is not clear, with
trials showing low and high doses as having similar
effects on mortality
Not certain whether any difference among the many
different ACE inhibitors out there today
Stages B, C, and D Heart Failure
Beta-blockers counteract the effects of the
sympathetic nervous system during heart failure
Beta-blockers improve survival, morbidity,
ejection fraction, remodeling, quality of life, rates
of hospitalization, and incidence of sudden
Should be used in select patients who are not
In those with asthma, DM with frequent
hypoglycemia, and bradycardia +/- heart blocks
should use caution
Stages B, C, and D Heart Failure
With beta-blockers one sees improvement
in systolic function even after 3 mos, with
reversal of remodeling after 4 mos
Carvedilol (nonspecific beta-blocker with
alpha effects) and metoprolol (beta-1
selective with no alpha effects) are
approved for the treatment of heart failure,
but the most prescribed med is atenolol
Stages B, C, and D Heart Failure
ARBs should be used for those who can
not tolerate ACE inhibitors, with trials
showing that ARBs have similar efficacy in
heart failure to ACE inhibitors
Stage C and D Heart Failure
Spironolactone, which blocks deleterious
effects of increased aldosterone (salt
retention, hypertrophy, etc), has been
shown to be helpful in patients with NYHA
class III or IV symptoms
Stage C and D Heart Failure
Diuretics are used to control congestion
Thiazide or loop diuretics often prescribed,
and combination therapy may be helpful in
advanced cases
Digoxin has no improvement in mortality,
but reduces rates of hospitalization and
worsening heart failure
Stage C and D Heart Failure
Biventricular pacemakers (where one lead is in the right
ventricle and the other is passed through the right
atrium, through the coronary sinus, and into a cardiac
vein on the lateral wall of the left ventricle) improves
ventricular synchrony
The pacemaker can be used to treat patients with heart
failure and a wide QRS
Effects include reverse remodeling (leading to decreased
heart size, improved EF, and decreased mitral
Exercise tolerance improves, as does quality of life, and
rate of hospitalization
Has not been shown to enhance survival
Stage C and D Heart Failure
Revascularization (either PCI or CABG):
– Improves symptoms
– Improves cardiac performance
– Reduces risk of sudden death
Mechanical devices (e.g. LVADs) are
continuing to evolve for patients awaiting
heart transplantation or as destination
AHA/ACC Recommendations
The following classification system has been
used by the AHA/ACC:
– Class I: conditions for which there is evidence and/or
general agreement that a given procedure/therapy is
useful and effective
– Class II: conditions for which there is conflicting
evidence and/or a divergence of opinion about the
usefulness/efficacy of performing the
– Class III: conditions for which there is evidence and/or
general agreement that a procedure/therapy is not
useful/effective and in some cases may be harmful
Specifically… ACE Inhibitors
Class I AHA/ACC recommendations:
– Stage A patients with a history of
atherosclerotic vascular disease, DM, or HTN
and associated CV risk factors
– Stage B patients with recent or remote history
of MI regardless of EF
– Stage B patients with reduced EF, whether or
not they have experienced an MI
– In all Stage C and D patients unless
ACE inhibitors
Target Dose
50 mg TID (SAVE trial)
10 mg BID (Delahaye et al. 2000)
40 mg QD (drug info)
40 mg QD (Packer et al. 1999 in
ATLAS trial)
40 mg QD (drug info)
10 mg QD (HOPE trial 2000)
Specifically… Beta-Blockers
Class I AHA/ACC recommendations:
– Stage B patients with recent MI regardless of
– Stage B patients with reduced EF, whether or
not they have experienced an MI
– Stable Stage C and D patients. They should
have no or minimal evidence of fluid retention
and have not recently required positive
inotropic agent
Target Dose
10 mg QD (CIBIS – II trial)
25 mg BID (US Carvedilol HF
150 mg QD (50 TID or 75 BID)
(Cleland 2003)
200 mg QD (MERIT-HF study)
succinate (XL)
100 mg QD (Ansari et al. 2003)
Relative contraindications for Bblocker use
Signs of peripheral hypoperfusion
PR interval>0.24
Second or third degree heart block
Severe COPD
Asthma history
Specifically… Spironolactone
Low doses of spironolactone given with an
ACE inhibitor in patients with class IV
symptoms reduced the risk of death and
Class IIa recommendations:
– Spironolactone in Stage C patients with
recent or current Class IV symptoms,
preserved renal function and a normal
potassium concentration
Specifically… ARBs
They should be considered instead of ACE
inhibitors due to intolerance.
Class IIa recommendations:
– In Stage C patients who are being treated
with digitalis, diuretics, and a beta-blocker
who cannot be given an ACE inhibitor
because of cough or angioedema
Specifically… diuretics
Class I indications:
– In Stage C and D patients who have evidence
of fluid retention
– In diastolic failure to control pulmonary
congestion and peripheral edema
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