HEART FAILURE

SEM. 4, 2010

Dr. TONY E. PARENGKUAN, Sp.JP

Bag. Kardiologi FK UHT Surabaya

Heart failure occurs when cardiac output and blood pressure are
inadequate for the bodys requirements.
The incidence increases with age and carries a poor prognosis.

USA :
> affects 3 million pts, 200.000 deaths, annually
> the annual incidence: 1-4 / 1000 population

Framingham study: 5-year mortality rate was`62% for men and

42% for women

London HF Study
> mean survival from diagnosis was 3 years
UK > HF, 5% of all hospital admissions

Left and right ventricular failure may

occur independently or together as
CHF/CCF

Forward failure refer to > symptoms and

signs relating to a poor cardiac output,
and backward failure > venous
congestion

Cardiac index:
- normal 2.5 - 4.0 L/min per m2
- CHF < 1.01 L/min per m2

 Diastolic

heart failure > may

have the symptoms and signs of
CHF but preserved systolic
function and a normal LVEF

High-output

failure (CO often >

10 L/min): sepsis, thyrotoxicosis,
large AV fistula, chronic
anaemia, beri-beri and severe
Paget's disease

AETIOLOGY

CAD
Hypertension
Valve disease
Cardiomyopathy: dilated > hypertrophic
Infiltrative: amyloid, sarcoid, iron, rarely
malignant
Infective: viral myocarditis, rheumatic
myocarditis, sepsis, infective endocarditis
with myocarditis
Collagen vascular disease
Drug induced: doxorubicin, daunorubicin,
5-FU
Metabolic and endocrine: mixoedema,
thyrotoxicosis, acromegaly,
phaeochromocytoma

AETIOLOGY

Toxins: alcohol
Radiation: myocardial fibrosis after
radiotherapy for breast Ca
Nutritional: beri-beri, kwashiorkor,
pellagra
Inherited: Fabry's disease, muscular
dystrophies, Friedreich's ataxia, glycogen
storage diseases
Hypersensitivity: anaphylactic shock
Cardiac transplant rejection
Incessant tachycardia
Miscellaneous: trauma, etc.

SYMPTOMS
Depend on

which ventricle is primarily

affected
the severity of the damage
aetiology

L V FAILURE

Fatigue and increasingly limited exercise

tolerance, exhaustion after even minor tasks,
dyspnoea in all its stages, orthopnoea and
paroxysrnal nocturnal dyspnoea
Dry nocturnal cough, cold peripheries,
palpitation, angina, giddiness or syncope on
effort; leaden sensation in legs on walking
Systemic embolism
Nocturia and reversed diurnal rhythms
Weight loss, muscle wasting and eventual
cachexia.

RV FAILURE
Peripheral oedema increasing to thigh
and sacral oedema, ascites and anasarca
Abdominal distension with ascites
Hepatic pain, especially on effort
Nausea and anorexia
Facial engorgement
Pulsation in face and neck (tricuspid
regurgitation)
Distended and even pulsatile varicose
veins
Epistaxes

Methods of Assessing Cardiovascular Disability

Sign
s An exhausted, ill-looking patient; dyspnoeic at rest or after minor effort.

Cool hands and feet with peripheral cyanosis; muscle wasting.

Blood pressure: low systolic pressure with low pulse pressure. Check no
paradox.

Raised JVP. Prominent systolic wave of TR. Kussmauls sign should be

negative. Prominent x and y descents in restrictive cardiomyopathy.
Prominent veins over shoulders, chest, abdomen and legs.

Low volume pulse. Resting tachycardia. Possible pulsus alternans. May be

in fast AF. Check for possible anacrotic pulse in occult aortic stenosis.

Displaced apex with LV dilatation. Thrusting apex of hypertensive heart

failure. May have high diffuse paradoxical apex of LV aneurysm. Systolic
apical thrill in ruptured mitral chordae. Double apex of LV hypertrophy in
sinus rhythm.

Signs

RV heave in pulmonary hypertension or with TR.

Severe MR may produce a sensation similar to
an RV heave as a result of systolic expansion of
the LA.

Auscultation: S3 gallop is the most important

sign of all. Signs of organic
aortic or mitral
valve disease. May just have functional mitral
and/or tricuspid pansystolic murmurs. In lowoutput states, murmur of severe aortic stenosis
may not be heard. Loud honking systolic
murmur of torn mitral xenograft or diastolic
murmur of torn aortic xenograft. More
continuous murmur of ruptured sinus of
Valsalva.

Signs
Smooth hepatomegaly. Pulsatile liver with TR.
Ascites with TR and RVF.
Leg oedema. Check sacral pad. Oedema is more easily
seen round the lower back than on anterior abdominal
wall.
Ventilation pattern: hyperventilation if in acute pulmonary
oedema. Cheyne-Stokes ventilation in a sedated patient
with a very low-output state.
Chest: bilateral basal effusions. Expiratory wheeze. Bubbly
cough. Fine basal crepitations are an unreliable sign of
pulmonary oedema. in addition check for signs of
possible infective endocarditis.

Catheter withdrawal from left ventricle (LV) to aorta (Ao) in a patient with LV
failure. There is a very high left ventricular end-diastolic pressure (LVEDP;
arrowed) of 50 mmHg. There is also pulses alternans in the peak LV
pressure and the aortic pressure trace.

DIFFERENTIAL DIAGNOSIS
Pulmonary Oedema
Mitral stenosis. cor triatriatum and atrial myxoma may all present in
pulmonary oedema with perfectly normal ventricular function. The
murmurs may be very difficult to hear in an acutely breathless
patient. Echocardiography is diagnostic.
Pulmonary oedema may occur with low LA pressures with sepsis,
noxious gas inhalation, severe myxoedema, hypoalbuminaemia, head
injury, subarachnoid haemorrhage or adult respiratory distress
syndrome.
RV Failure
The most important differential is from pericardial constriction. Also
consider SVC obstruction (non-pulsatile neck veins), malignant
ascites with liver secondaris, nephrolic syndrome and pelvic nodes
causing lymphatic obstruction, and leg oedema

Acute pulmonary oedema: 'batswing' appearance.

Note small heart. Restrictive cardiomyopathy.

Concepts of Treatment

Neuroendocrine Activation

In heart failure there is an inappropriately raised

systemic
vascular resistance caused by a combination of
sympathetic overdrive and activation of the renin angiotensin system.
Neuroendocrine activation results in raised levels of
angiotensin ll, noradrenaline and arginine vasopressin
(antidiuretic hormone, ADH).
Endotellin levels (released from vascular endothelium)
are
also raised in heart failure, contributing to the
vasoconstriction.

Concepts of Treatment

Natriuretic Peptides

Raised levels of atrial natriuretic peptide (ANP) and brain natriuretic

peptide (BNP)
also occur in heart failure.
They promote a natriuresis and arterial and venous dilatation, and inhibit
ADH
and aldosterone release. However, their effects are overwhelmed by the
other
neuroendocrine activation mechanisms.
B-type natriuretic peptide is synthesized by myocardial cells in response to
raised
ventricular filling pressure.
The clinical picture must be taken into account. Levels > 100 pg/ ml indicate
heart failure and this cut-off level is a very sensitive (>90%) and specific
(>76%)
test, helping to differentiate pulmonary from cardiac causes of dyspnoea.
In severe heart failure levels are much higher. High BNP levels carry a poor
prognosis (eg. >300 pg/ml), particularly if levels do not fall on treatment.

Cardiac Failure Treatment

Heart failure is managed with bed rest, diuretics

and vasodilating agents.
The use of inotropes to flog a failing heart raises
problems other than increasing cardiac work.
No oral agent other than digoxin has been shown
to be safe and effective in long-term trials

Cardiac Failure Treatment

Vasodilators are divided into three groups

1.

Venodilators: reduce preload by dilating venous

capacitance vessels, eg. nitrates, some diuretics. They
lower filling pressures without initially much improvement
in stroke volume. At higher doses they also become
arterial dilators.

2.

Arterial dilators: reduce afterload. Dilate arterial

resistance vessels, e.g. hydralazine. They improve stroke
volume without much reduction in filling pressure or
pulmonary venous pressure.

3.

Combined arterial and venous dilators: drugs such as

nitroprusside and -blocking agents. These improve
stroke volume and reduce filling pressure. They are very
useful in LVF.

A wide variety of vasodilating drugs are now available.

Choice of Vasodilators
LV Failure (Acute) with Pulmonary Oedema
and
Normotension
Examples are acute mitral regurgitation, septal
infarction with
VSD; acute infarction in normotensive patient:
nitroprusside: it full haemodynamic monitoring
available, with intravenous furosemide.
lf no monitoring facilities available other than ECC:
furosemide i.v. + isosorbide dinitrate or glyceryl
trinitrate i.v., then
oral isosorbicle dinitrate + ACE inhibitor + oral
diuretic as the patient improves.

Choice of Vasodilators

Low-output States
Hypotensive, cool, oligaemic patients (socalled 'forward
failure'):

Dopamine, monitoring haemodynamics.

Once normotension is restored, addition
of nitroprusside may be beneficial. Alternatively dobutamine if urine output
satisfactory.

Choice of Vasodilators

Chronic CCF (Oral Therapy Only] in

Combination

Furosemide (+ amiloride or
spironolactone) if hypokalaemic
ACE inhibitor, especially if hypertensive
Long-acting nitrate once or twice daily
Digoxin if in AF, large heart on chest
radiograph or audible S3;
Warfarin if large heart or in AF
No added salt to food (allow a little for
cooking in most cases).

Diastolic Heart Failure

(Heart Failure with Preserved Systolic Function)
Some patients may have all the symptoms of cardiac failure but
a
normal LVEF on echocardiography (>50%) and a normal size
heart
on the chest radiograph.
A wide variety of cardiac conditions may cause this picture:
Incorrect assessment of LVEF
Valvular heart disease (e.g. aortic stenosis, acute mitral
regurgitation)
Restrictive cardiomyopathy
Pericardial constriction
Systemic hypertension
IHD
Atrial myxoma
Idiopathic diastolic dysfunction.

Management of Diastolic Heart Failure

Management of these cases depends on the aetiology

of the stiff ventricle.
Vigorous control of hypertension is important.
Diuretics, salt restriction and ACE inhibitors are
helpful for symptom control.
Maintenance of sinus rhythm is important because
atrial transport helps maintain cardiac output and
rapid deterioration occurs with the development of
AF. Urgent DC cardioversion may be needed, and also
amiodarone and an electrophysiological opinion. lf
the LA <6.0 cm on echocardiography RF ablation of
the AF maybe a possibility.
Revascularization may be needed for the ischaemic
left ventricle.
Slow-release yerapamil may be helpful in idiopathic
cases.

Effects of beta blockade on the ischemic heart. Beta blockade has a beneficial effect on
ischemic myocardium unless (1)

BETA-ADRENOCEPTOR BLOCKING AGENTS

Characteristic

Atenolol

Usual
Maintenance
dose

50-100
mg/d

Metoprolol/
XL
50-100 mg
b.i.d.-q.i.d.
/50-400
mg/d

Nadolol

Pindolol

40-80 mg/d

10-40 mg/d
(b.i.d.-t.i.d.)

Propranolol
/LA
80-320
mg/d
(b.i.d.-t.i.d.)
/80-160
mg/d

Timolol

Acebutolol

10-30 mg
b.i.d.

200-600 mg
b.i.d.

Labetalol

Bisoprolol

Betaxolol

Carteolol

Penbutolol

Carvedilol

Esmolol (IV)

Sotalol

100-400 mg
b.i.d.

5-20 mg/d

5-20 mg/d

2.5-10 mg/d

10-40 mg/d

3.125-50 mg
/b.i.d.

Bolus of 500
g/kg;
infusion at
50-200 mg
/kg/min

80-160 mg
b.i.d.

CALSIUM ANTAGONISTS
Characteristic

Diltiazem/SR

Nicardipine

Nifedipine/SR

Usual adult dose

IV: 0.25 mg/kg

bolus, then
5-15 mg/hr

IV: 3-15 mg/hr

Oral: 10-30 mg t.i.d.

Oral: 30-90 mg
t.i.d.-q.i.d.

Oral: 20-40 mg
t.i.d.

SR: 90 mg/d

SR: 60-180 mg
b.i.d.

SR: 30-60 mg
b.i.d.

CD: 120-480
mg/d

Verapamil/
SR

Amlodipine

Felodipine

Isradipine

Nisoldipine

IV: 0.075-0.15
mg/kg

Oral: 2.5-10
mg/d

Oral SR: 2.510 mg/d

Oral CR: 2.510 mg

b.i.d.

Oral SR: 1040 mg/d