Systolic Heart Failure

Types of Heart Failure

Systolic heart failure - failure of
contraction
Diastolic heart failure- failure of
relaxation
This lecture concentrates on systolic
heart failure

Staging system of Heart

Failure
A - patients at risk, but no structural or
functional defects, (CAD,HTN, DM,
metabolic syndrome, obesity)
B - pts with structural heart disease but
do not manifest symptoms of heart
failure (LV enlargement or dysfunction,
LVH, valvular heart disease)

Staging system of Heart

Failure
C - pts with prior or current symptoms
that can be controlled with standard
medications
D - pts with severe disease, frequent
hospitalizations, often requiring
advanced therapies

NYHA Functional
Classification
Class I - pts with disease but no symptoms that
limit activity
Class II - pts with slight limitations of physical
activity related to symptoms of HF (dyspnea,
fatigue)
Class III - pts with marked limitations of
physical activity, but no symptoms at rest
Class IV- pts cannot carry out any physical
activity without limitation and may have
symptoms even at rest

Systolic Heart Failure

Backward failure theory
Decreased contractility results in increased
LV diastolic pressure causing fluid build up
in the pulmonary vasculature.
Symptoms include dyspnea, orthopnea,
abdominal fullness, leg swelling
Signs include JVD, gallops(S3), MR/TR
murmurs, rales, peripheral edema

Systolic Heart Failure

Forward failure theory
Inadequate cardiac output at rest or with
exercise stress results in decreased
perfusion to vital organs
Symptoms include fatigue, weakness,
dizziness, poor mentation, anorexia,
nausea
Signs include pallor, cold extremities,
tachycardia, hypotension

 Initial insult (AMI etc) causes changes in

neurohormonal profile and direct myocyte
changes
Causes myocyte hypertrophy and impairs myocyte
function
End result is chamber remodeling which causes
progression in ventricular dysfunction and HF

Key Neurohormonal Mediators

Bad Players

Norepinephrine
Angiotensin II
Aldosterone
Endothelin
Vasopressin
Tumor necrosis
factor

Good Players
Natriuretic peptides
Nitric oxide
prostacyclin

 Bad players stimulate hypertrophy,

cause remodeling, fibrosis, apoptosis
and contraction abnormalities
This leads to vasoconstriction, sodium and
fluid retention

 Good players are antihypertrophic,

antiproliferative and vasodilatory
They result in reverse remodeling and
encourage diuresis

 Etiologies:

CAD (65%)
Idiopathic dilated cardiomyopathy
Alcoholic/toxin-induced cardiomyopathy
Infectious/Inflammatory process
Familial dilated cardiomyopathy
Peripartum cardiomyopathy
Stress-induced cardiomyopathy
Endocrine/Nutritional causes
Iron overload cardiomyopathy
Tachycardia mediated cardiomyopathy

Etiologies
CAD
Most common cause (65%)
Reversible
Revascularization can markedly improve
outcomes

Etiologies
Idiopathic dilated cardiomyopathy
Diagnosed when all other causes have
been excluded

Etiologies
Alcohol/toxin induced cardiomyopathy
Alcoholic CM prevalence is estimated at
20% of all DCM
Alcohol has a direct acute and chronic
toxic effects on the myocardium (> 7
drinks/day for >5 years)
Cocaine and other catecholaminergic
drugs
Chemotherapeutic drugs (anthracyclines)

Etiologies
Infectious/Inflammatory
Coxsackie B(#1)
HIV, mycoplasma, HCV, Lyme
Chagas disease, endemic in South and
Central America
Lupus, scleroderma, RA, Kawasaki, ChurgStrauss and others

Etiologies
Familial dilated cardiomyopathy
at least 20-30% of all DCM
Can be autosomal dominant or recessive, Xlinked, or mitochondrial
Associated with myscular dystrophies

Etiologies
Peripartum cardiomyopathy
Development of clincal HF in the last
month of pregnancy or the first 5 months
after peripartum
Half of all women normalize within 6
months and have a good prognosis
NO ACE/ARB if pregnant or breast feeding

Etiologies
Stress-induced cardiomyopathy
Other names include tako-tsubo, apical ballooning,
or broken heart syndrome
Reversible cause of acute systolic dysfunction
resembles a large anterior wall MI
Associated with emotional, surgical, or dramatic
stresses and catecholamine surge
Improves over days to weeks, usually with
complete resolution of LV function

Etiologies
Endocrine/Nutritional causes
Rare
Hypothyroidism/thyrotoxicosis
Diabetes/obesity (risks, stage A)
Acromegaly and GH deficiency
Pheochromocytoma
Thiamine (wet beriberi - high output form)
Carnitine, selenium

Etiologies
Iron overload cardiomyopathy
Can be primary (hereditary) or secondary
Hereditary hemochromatosis is common in
Northern Europeans and results in iron
deposition in the heart, joints, liver, skin
(bronze diabetes)
Gold standard for diagnosis is liver biopsy

Etiologies
Tachycardia mediated cardiomyopathy
Often difficult to discern whether
tachycardia is primary force driving the
cardiomyopathy or secondary
phenomenon
Treatment of heart rate improves and can
normalize LV function
Pharmacologic, cardioversion, or ablation

Clinical Evaluation
History

Symptoms and functional class

Angina
Arrhythmias
Alcohol history
Past medical history (chemo etc)
Evaluate volume status

Clinical Evaluation
Physical

Volume status
Hemodynamics
Murmurs
Vitals with orthostatics

Clinical Evaluation
Laboratory

Chemistries
Renal function
CBC with dif
LFT
TSH
HbA1c
Lipids
BNP

Clinical Evaluation
Studies
CXR
ECG (Holter)
Echocardiogram

Clinical Evaluation
Rule out CAD since it is the most
common cause and is reversible
Patients should have angiography if the
have angina or known ischemia, or if they
have a high likelihood of CAD

Clinical Evaluation
Endomyocardial biopsy is not part of a
routine evaluation
It is only useful if the results will influence
therapy, such as in the following conditions

Sarcoidosis, amyloidosis
Hypereosinophillic syndrome
Fulminant myocarditis
Giant cell myocarditis
Drug toxicities

Management
Any patient who presents with first
either the first episode of heart failure or
with acute decompensation of
previously stable heart failure they
should be evaluated for the cause of
their deterioration

Clinical Evaluation
Drugs to avoid in heart failure
NSAIDs
Most antiarrhythmics
Most calcium channel blockers (felodipine,
amlodipine are likely safe)
thiazolidinediones

Management
Drugs in Heart Failure
Diuretics
loop diuuretics are preferred over thiazides if
renal function is impaired

Management
Drugs in Heart Failure
ACE inhibitors
ACE inhibitiors, start at low dose and titrate
slowly following creatinine and potassium levels
ACE inhibitors are first line, but ARB may be used
instead if history of cough or angioedema
Evidence is soft for addition of ARB to ACE

Management
Drugs in Heart Failure
Beta blockers
carvedilol, metoprolol, succinate and bisoprolol)
Start low and titrate slowly
Relative contraindications include reactive
airway disease, aymptomatic bradycardia, SM
with recurrent hypoglycemia, resting limb
ischemia

Management
Drugs in Heart Failure
Aldosterone antagonists

Cautious use in patients with Creat >1.5 or K >5

Closely follow K and Cr
Avoid K and salt substitutes
Patients must urgently address dehydration secondary to
the risk of renal failure
Limited study populations
NYHA III-IV
Post-MI with reduced EF and symptoms or DM

Management
Drugs in Heart Failure
Digoxin
Symptomatic improvement with reduced
hospitalizations in patients with mild to
moderate heart failure
Less effective in women than men
Optimal target level is 0.6 - 0.9, above which
there is an increase in mortality
Drug interactions: amiodarone

Management
Drugs in Heart Failure
Nitrate-Hydralazine
Inferior to ACE/ARB but should be used for
patients who are intolerant of these drugs
Should be used in addition to ACE-I and beta
blockers in African-American patients who have
persistent NYHA class II-IV symptoms

Management
Drugs in Heart Failure
Warfarin may be sued in patients with low
ejection fraction and

Atrial fibillation
Intracardiac thrombus
Previous thromboembolism
Prophylactic use is controversial

Management
Drugs in Heart Failure
Aspirin if the patient has ischemic
cardiomyopathy or atherosclerotic vascular
disease
If the patient has non-ischemic
cardiomyopathy do not use aspirin

Management
Non-pharmacologic treatment
Nutritional counseling regarding sodium
restriction, fluid restriction and alcohol
Daily weight and symptom assessment
with an understanding of how to take action
if there is a change
Regular physical activity
Education on the importance of compliance

Device Therapy
ICD
Half of pts with HF die suddenly from
arrhythmias
Implantation of and internal cardioverter
defibrillator may improve survival in centain
subsets of patients

Device Therapy
Cardiac resynchronization therapy
Used for patients with a conduction delay,
meaning the walls of the ventricle contract
at different times
Allows contraction of the ventricle to be
more efficient because it forces all walls of
the heart to contract at the same time

Management
Device Therapy
ICD
EF < 30-35%
History of inducible arrhythmia, sudden cardiac
death

BiVentricular pacemaker
QRS >120
EF< 35%
NYHA III-IV

Guidelines
Chronic stable Heart Failure Therapy
Stage A:
Treat all underlying disorders, such as HTN,
DM, lipids, thyroid dysfunction and CAD
Modify all social factors, such as alcohol, diet,
smoking
Consider starting ACE-I if patient has diabetes,
CAD or HTN

Guidelines
Chronic stable Heart Failure Therapy
Stage B:
All therapies listed under stage A
Utilize beta blocker and ACE-I in all patients with a
history of AMI or any patient with reduced EF
Evaluate patients for valvular heart disease and
recommend surgery for any hemodynamically significant
valvular disorders
Consider ICD for patients after AMI with EF < 30%

Guidelines
Chronic Stable Heart Failure Therapy
Stage C:
All therapies listed under stages A and B
Aldosterone antagonists should be started in patients with
NYHA III-IV and a reduced EF
Institute diuretics and salt/fluid restriction
Consider the addition of hydralazine/imdur in AfricanAmerican patients, may also be used in place of ACE-I in
patients unable to take ACE-I
Consider digoxin in patients with symptoms and EF<30%
ICD if EF<30-35%
CRT if EF<35%, NYHA III-IV, QRS>120

Guidelines
Refractory Heart Failure
Stage D
All therapies listed under stages A, B and C
Refer eligible patients for transplant/heart
failure center
Consider LVAD for destination therapy
Consider Swan placement to guide therapy
End-of-life care should be discussed, including
option of deactivating ICD

Management
Acute Decompensated Heart Failure
Patients need to be evaulated regarding
congestion(wet versus dry) and for
adequate perfusion (cold versus warm)
Most patients are wet and warm, others
may be in shock and are wet and cold

Management
Acute Decompensated Heart Failure
Wet and warm treatment
Diuresis
vasodilators

Management
Acute Decompensated Heart Failure
Wet and warm treatment
Diuresis
inotropes
vasodilators

Management
ADHF: Vasolilators
Nitroprusside
Arterioral and venodilator, avoid in ischemic patients

Nitroglycerin
Primarily venodilator, best if ischemie cause of HF

Nesiritide
Allows for diuresis and improved relaxation, concerns for
mortailiuty and dosing

Management
ADHF: inotropes
Milrinone/Dobutamine
Limited role
Use with low output state with marginal
blood pressure despite adequate filling
pressure
Risk of tachyarrhythmias and hypotension

Management
ADHF Device therapy
LVAD(left ventricular assist device), device
connected to the left ventricle to
mechanically pump blood and rest the
heart
Ventricular reconstruction surgery
Heart transplant

LVAD

Case 1
55 year old male presents with mild dyspnea
on exertion. He denies angina or dizziness.
There is no significant past medical history.
He drinks 2-3 glasses of wine per week
On physical exam BP 134/70, HR 125. There
is no JVD. Lungs are clear. Heart is
tachycardic with irregular rhythm. Routine
labs are normal. EKG shows AF. Echo
demonstrates global hypokinesis with ejection
fraction of 35%

What is the patients NYHA functional

class
A.
B.
C.
D.

I
II
III
IV

What is the patients heart failure stage

A.
B.
C.
D.

A
B
C
D

What do you recommend for this

patient
A. Admit to hospital for IV diuresis
B. Encourage him to stop drinking alcohol
and re-evaluate in 6 months
C. Admit to hospital for endomyocardial
biopsy
D. Start a medication to slow heart rate

71 yo male with known reduced EF presents to

ER with worsening dyspnea and new orthopnea.
BP is 150/80, he has elevated JVP, bibasilar
rales and lower extremity edema. EKG shows
ischemic changes with ST segment depression.
Which drug is most useful in addition to diuretics
A.
B.
C.
D.

Nitroglycerin
Milrinone
Dobutamine
diltiazem

1.
2.
3.
4.
5.

68 yo male with EF 35% presents to clinic. His

is asymptomatic on furosemide 20mg daily. He
is on no other medications. Which is the next
best step
Increase furosemide to 40mg
Add nitrate/hydralazine combination
Add high dose atenolol
Add low dose lisinopril and low dose carvedilol
Make no changes

 Which of the following patients is a

good candidate for ARB therapy
45 yo with K> 6.0 on lisinopril
65 yo with HF but on no medications
56 yo with occasional nocturnal cough on
lisinopril
None of the above