CARDIOLOGY1

CONGESTIVE HEART
FAILURE
Causes of Heart Failure
Predominant systolic failure
1. Coronary artery disease
2. Hypertension
3. Dilated Cardiomyopathy (idiopathic, toxic,
infectious)
Predominant diastolic failure
1. Hypertension
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy (amyloidosis, sarcoid)
4. Constrictive pericarditis
5. High output failure

Interruption of the renin angiotensin-aldosterone

axis by means of an ACE inhibitor SVR,
afterload cardiac output in HF.
ADH: released because the kidneys are now seeing an
effective in blood flow. Thus H2O and salt
retention occurs.
Endothelin: also released in HF marked
vasoconstriction.
Atrial natiuretic peptide: counter regulatory protein
that assist in combating the vasoconstriction.

Forms of HF
Backward heart failure

Inability of cardiac muscle to shorten against a load

alters the relationship between ventricular endsystolic pressure and volume. The following
adaptations take place:
1. ventricular end-systolic volume ventricular endVentricular Function
systolic pressure
Heart failure (HF) is often associated with impaired
ventricular function. Muscle removed from patients 2. volume and pressure in the atrium behind the
failing ventricle.
and animals with HF shows a in the active length
tension relationship and icular function curve. In the 3. atrium contracts more vigorously
presence of a disturbance in myocardial contraction 4. pressure in the venous and capillary beds behind
(and upstream) to the failing ventricle .
or an excessive Lamic burden placed on the
5. transudation of fluid from the capillary bed into the
ventricle or both, the heart depends upon :
interstitial space leading to pulmonary congestion
1. Frank-Starling mechanism: preload (i.e.,
and/or peripheral edema and ascites.
lengthening of sarcomeres provides an optimal
Although an in LVEDP is associated with
overlap between thick and thin myofilaments) acts
ventricular function, pressure is not specific for
to sustain cardiac performance
HF and there is no upper limit value specific for LV
2. release of catecholamines by adrenergic nerves
failure. LVDP may by other factors such as
and the adrenal medulla myocardial
compliance, severe volume overloading (mitral
contractility
regurgitation), or cardiac tamponade.
3. Myocardial hypertrophy: w/or w/out chamber
dilatation in which the mass of contractile tissue is
Forward Failure Hypothesis.
augmented.
Clinical manifestations of HF inadequate delivery of
Initially these 3 compensatory mechanisms may be
blood into the arterial system manifestations due
adequate to maintain the overall pumping ability of
to CO perfusion of vital organs, including:
the heart. However, these compensatory
1. brain mental obtundation
mechanisms have a limited potential, and if the
2. skeletal muscles weakness
disturbance in myocardial contraction and / or the
excessive hemodynamic burden persists, the heart
3. kidneys Na and H2O retention
ultimately fails.
Although CO is frequently in HF, failure cannot be
defined by a minimum value of CO. For instance,
Alterations in the function of the
CO at rest may be normal even when the heart is
Neurohumoral system
failing.
Adrenergic nervous system:
An enlarged heart may produce the same SV with
Positive inotropic effect mediated by its interaction with
ejection fraction.
the cardiac sarcolemmal -receptor which with the
A CO may be above normal, as in cardiac failure
help of G proteins stimulate production of
associated with sever anemia or severe
adenlylate cyclase formation of cAMP.
hyperthyroidism (high output failure).
intracellular cAMP activates cAMP-dependent
Right sided versus left sided failure
protein kinases catalyze transfer of phosphate
Fluid localizes behind the specific cardiac chamber that
groups to specific sites on other intracellular
is initially affected. Thus, symptoms secondary to
proteins transcellular Ca influx through slow
pulmonary congestion predominate in patients with
channels in response to depolarization, as well as
myocardial infarction, hypertension, aortic and
release, faster reaccumulation and storage of Ca in
mitral valve disease (left heart failure). With time,
the sarcoplasmic reticulum.
fluid accumulation becomes generalized and ankle
While circulating catecholamines may help to maintain
edema, congestive hepatomegaly, and ascites occurs
ventricular function for variable periods of time,
(right heart failure).
there is a price to be paid worsened survival.
The most common cause of right heart failure is left
Decompensation may be due to the ability of
heart failure.
catecholamines to:
Systolic versus diastolic
1. cause necrosis and/or apoptosis
2. regulate the -receptor-G protein-adenlylate
Diastolic failure is impaired capacity to accept blood or
cyclase complex
fill without a compensatory increase in LAP. It may
3. cause arrhythmia.
be the sole cause of HF in 1/3 of pts. Unlike systolic
dysfunction, in diastolic dysfunction, LV is usually
Renin-angiotensin-aldosterone system:
small and thick, with a good overall ejection
In low-output states activation of the reninfraction. Diastolic dysfunction may be seen in
angiotensin-aldosterone axis. While there are several
ischemic heart disease, HTN, LVH, and infiltrative
signals for renin release, renin conversion of
diseases. Some patients with systolic dysfunction
angiotensin 1. Angiotensin II is then formed by
also have a component of diastolic dysfunction
ACE.
Angiotensin II: potent vasoconstrictor. Contributes to
extreme of systemic vascular resistance.

Precipitating Causes of CHF

2CARDIOLOGY
1. Inappropriate treatment reductions or additions,
(salt, beta blockers, estrogens)
2. Arrhythmias:
Tachyarrhythmias: time available for ventricular
filling, O2 consumption ischemia
Bradycardia: SV is max and cant further CO
3. Late complications from an MI: papillary muscle
dysfunction
4. infections: metabolic rate, fever, tachycardia

Cardiac Auscultation

S-1 is related to the closure of the mitral valve.

S-2 to the closure of first the aortic. Then the pulmonary
valves.
Normally silent opening of the aortic and pulmonary
valves, and mitral and tricuspid valves is.
Abnormal Findings:
S-3 in adults w/enlargement and HF: In early diastole,
rapid ventricular filling takes place. In young adults,
this is signaled by an audible S-3. If in adults
collaborates the diagnosis of HF. Associated with
cardiac dilatation.
Loud S-4: Sign of ventricular diastolic compliance.
Normally, blood flows rapidly from the atrium to
Dyspnea
ventricle in early diastole. Thereafter, occurs the
1. Pulmonary congestion is associated with dyspnea
period of diastasis during which time little or no
(difficult or labored breathing) only with exertion in
blood flows from the atrium to ventricle. Atrial
mild heart failure. W/worse HF progressively less
contraction causes a 2nd spurt of blood flow from
exertion and finally even at rest.
atrium to ventricle. When ventricular diastolic
2. Orthopnea: When a subject is supine, the fraction of
compliance is , atrial systole is accompanied by a
the blood volume contained in the lungs is .
loud S-4 sound which occurs in pre-systole.
3. PND: In its worst form, it is accompanied by cough,
sometimes productive of white frothy sputum which Pansystolic mumur: When the ventricles dilate, the AV
valves may become incompetent. This permits blood
is occasionally blood stained. These attacks are
to regurgitate from the ventricle to the atrium. A
termed pulmonary edema.
pressure gradient from ventricle atrium exists
4. Cough: 1 a respiratory symptom. However cough,
throughout systole pansystolic mumur.
on assuming the supine position or on performing
exercise, is an important symptom of cardiac disease JVP
and is related to pulmonary congestion.
The deep jugular veins are not separated from the

Symptoms related to pulmonary

congestion

Other Evidence of Pulmonary Congestion

W/ pulmonary congestion can hear on PE.

Chest X-ray: Redistribution of the blood in the lungs
engorgement of the pulmonary veins and to fluid in
the interstitial spaces of the lungs or in the alveoli.
Normal standing subject:
upper lung zones are lucent (blood flow is least and
the veins are almost collapsed)
blood lower lung zones flow is greatest.
In HF normal distribution of blood flow from top
bottom of the lungs is abolished and eventually even
reversed in cardiac failure in appearance of
lung fields on X-ray.
Enlarged heart: most forms of HF cardiac
enlargement. See an enlarged heart on X-ray. If a
patient presents with new onset severe CHF and a
normal heart size, think of a recent AMI.

Systemic Congestion
Pulmonary circulation: Normally pressure,
capacitance system. 5-10 mmHg suffices to drive
blood from the head of the pulmonary circulation
(the pulmonary artery ) to its termination (the left
atrium).
If LV diastolic pressure pulmonary venous
pressure (from 10-30 mmHg), normal mean
pulmonary arterial pressure of approximately 11
mmHg will not suffice to perfuse the pulmonary
vascular bed. Then obligatory pulmonary arterial
HTN accompanies LVD HTN.
systolic RVAP hypertrophy and dilate and failure
RVD pressure transmitted throughout
diastole through the open tricuspid valve to RA
SVC and IVC (not separated by valves from the
right atrium) in CVP congestion of systemic
tissues and organ:
1. liver becomes congested and eventually its function
is grossly impaired
2. subcutaneous fluid appears as edema
3. effusions in the peritoneum (ascites) and in the
pleural and pericardial cavities.

Cardiac Manifestations of HF
Heart Enlargement: Manifested by clinical
examination, the chest radiograph, the
electrocardiogram, and the echocardiogram.

1.
2.
3.
4.
5.

superior vena cava by valves, so that the level of the

central venous pressure may be noted by observing
the jugular venous pulsations. Jugular venous
pulsations ought not be visible above the level of the
angle of Louis in any posture supervened above 30
degrees.
A wave: generated by atrial systole
C wave: Associated with isovolumic systole
X descent: accompanies ventricular ejection
V wave: passive filling of the atrium from its
supplying veins
Y descent: opening of the tricuspid valve.

When the RV fails, JVP is . Rt ventricle dilation

1. large systolic v wave in the JVP
2. y wave, is precipitous

HR and Rhythm; BP
Hypoperfusion sympathetic stimulation
tachycardia which may partially correct CO
related to SV.
Sympathetically mediated vasoconstriction mild
HTN. LA HTN and stretching to A. fib.
Extensive myocardial dz ventricular extrasystoles
and occasionally ventricular tachycardia.

Regional Perfusion
HF CO (esp. during exercise). Major redistribution
of regional perfusion occurs.
1. in renal blood flow retention of Na and H2O
blood volume dilation of the heart, of
ventricular diastolic pressures, and congestion of the
lungs and systemic tissues.
2. capillary pressure (pulmonary and systemic)
moves fluid from the vascular compartment to the
tissues.

Routine tests for heart failure.

ECG: AMI, arrhythmias, heart block.
Chest x-ray: described above
Echo: allows us to see the size of the heart, the function,
and the thickness and any vascular abnormalities.

Treatment Goals of Cardiac

Failure
Improve symptoms
Prevent deterioration of function

CARDIOLOGY3
survival.

Non-pharmacologic
1. Removal or treatment of precipitating or
aggravating causes:
2. treating respiratory or other infections
3. management of arrhythmias
4. Treatment of HTN
5. Treatment of MI.
6. Control risk factors for myocardial ischemia.
Diet. Restriction of Sodium Intake- a daily sodium
intake of 2 to 3 grams can be quite tolerable with
food additives to improve palatability. Salt binges
are a major reason that patients decompensated.
Physical activities: because restricting exercise causes
reconditioning and regular exercise can increase
peak exercise capacity, encouraging patients to
exercise regularly and as strenuously as their
symptoms permit, or to enter into formal
rehabilitation programs can enhance their quality of
life.

Hydralazine
Afterload and is therefore used for SVR and HTN.
In combination w/nitrates survival in patients with
CHF. Work well to mitral regurgitation or aortic
insufficiency. More SE than ACE inhibitors.
Nitrates
Mostly venodilation with some afterload .
Complement diuretics in right and left atrial pressures.
Especially useful if coronary artery dz is present.
They are available orally or as a patch.
Tolerance to its effects have become an issue and to
prevent this, a "nitrate free interval" should be
instituted (3x/day vs. 4X/day).

ACE inhibitors

Most important advance in therapeutics for HF in the

past two decades.
Up to a 40% in 1-year mortality in class IV pts.
1. Slows remodeling (ventricular enlargement)
2. hemodynamics and survival rates in patients with
LV dysfunction due MI.
3. Prevent clinical deterioration in asymptomatic
Cardiac transplantation:
patients with ejection fractions.
1. Candidates should be < 60 y.o.
2. Advanced CHF
4. 1st line therapy for all patients with LV function.
3. Strong psychosocial support system,
Even mildly symptomatic patients who used to do
4. Exhausted all other therapeutic options,
fine just on a diuretic should now also receive an
5. Free of irreversible extra cardiac organ dysfunction
ACE inhibitor.
that would limit functional recovery or predispose to ACE inhibitors should be instituted with caution if there
post-transplant complications.
is renal dysfunction or hyperkalemia. While ACE
Survival is 90% at 1 year and 70% at Lye years.
inhibitors can cause a cough, many patients with
CHF also have cough.
Angiotensin II receptor antagonists: losarten, valsarten.
In contrast to ACE inhibitors. No bradykinin
Diuretics:
levels cough and angioedema.
filling pressures of the heart but does not bring the
Calcium channel blockers
patient to a new Starling curve (no increase in
Verapamil, nifedapine, diltiazem: 1st generation drugs.
cardiac output).
Vasodilation counterbalanced by negative inotropic
Choice of appropriate diuretic agent:
effects. Not well tolerated in congestive heart
1. Mild sodium retention-Thiazides.
failure.
2. Moderate to sever sodium retention--loop diuretics
Amlodipine and felodipine: 2nd generation drugs.
(furosemide (lasix) bemetarnde (bumex).
Vascular specific. symptoms.
3. Persistent sodium retention--loop diuretics plus
thiazides or metolazone.
Inotropic agents
4. K+ sparing diuretics (spironolactone) may also be
Digitalis
added.
The only approved oral inotropic drug.
Diuretic dose should be titrated to relieve congestive
Most useful with moderate CHF, esp. in the setting of A.
symptoms and signs, normalize CVP, and stabilize
fib.
weight. Side effects include intravascular volume
Least useful in cardiogenic shock with pulmonary
depletion, hyponatremia, hypokalemia,
edema. Up to 25% of hospitalized patients get toxic.
hyperkalemia, metabolic alkalosis, hyperuricemia
Toxicity most often occurs in the setting of old age,
renal failure, COPD, hypokalemia, hypocalcemia,
Pearls concerning diuretics:
hypothyroidism, and some drugs such as quinidine,
1. It's generally better to give HCTZ or lasix as a
verapamil and amiodarone.
single daily dose. If inadequate, more diuresis will
usually be obtained by doubling the dose rather than
Other inotropes have been tested, including beta
giving the same dose twice.
agonists, dopamine like drugs and hospodiesterase
2. Avoid excessive diuresis that might prevent titrating
inhibitors. While short term improvement has been
ACE inhibitors to full therapeutic levels.
seen, tachyflaxis and long term side effects
3. Check serum K frequently during initiation and
(including increased mortality) currently preclude
titration (about every 3 days)
their use.
4. Beware of combo of ACE inhibitor and K sparing
agents.
5. If large doses of diuretics are used, Mg levels should Parenteral inotropes have been used with much success
for decompensated patients. These drugs include:
be checked.
1. Dobutamine: -agonist. CO, wedge pressure at
6. Pt adjustment of dose: Since the need for diuretics
doses that don't HR and BP.
varies depending on the patient's diet and level of
activity, having patient adjust the dosage themselves 2. Milrinone: phosphodiesterase inhibitor. Both
inotropic and vasodilatory effects.
is a useful approach. Pt can be advised to or
their diuretic dose to maintain their weight-as
-Blockers:
measured each morning--titrate to a range in which
Some success in moderately severe CHF.
they have few symptoms of congestion.
Start with doses and titrate slowly in a compliant
Vasodilators
patient.
Always used in patients w/CHF.
Cavedilol: Newer -blockers may offer even better
Most offer venodilation and/or arterial vasodilation.
results. Selective -blocker with -1 blocking
Most effective when pulmonary congestion is 2 to
effects. Also anti-oxidant effects. function,
pulmonary wedge pressure rather than CO.

Drug Treatment of HF

4CARDIOLOGY
symptoms, and survival in all but class IV patients
with CHF.
Should be instituted (with a cardiologist) at 3.125 mg
bid and doubled every 2 weeks up until 25-50 bid.