Transcript Definition, Heart failure, epidemiology, pathophysiology, Types of

This lecture was conducted during the Nephrology Unit
Grand Ground by Medical Student rotated under
Nephrology Division under the supervision and
administration of Prof. Jamal Al Wakeel, Head of
Nephrology Unit, Department of Medicine and Dr.
Abdulkareem Al Suwaida, Chairman of Department of
Medicine. Nephrology Division is not responsible for the
content of the presentation for it is intended for learning
and /or education purpose only.
Heart failure
Presented by:
Dr.Khadra Al-Somali
Medical Student
27-8-2008
Definition
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Definition:
Heart failure is the
inability of the
heart to maintain an
output adequate to
meet the metabolic
demands of the
body.
Heart failure.
It is associated with extremely
high morbidity and mortality. It is
a syndrome and not a disease .
Epidemiology:
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About 5million cases of heart failure are
prevalent in the US.
Incidence is estimated at 550,000 cases
per year.
The 5 year mortality rate following
diagnosis with heart failure is almost
50%.
Pathophysiology:
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When the heart fails, considerable
changes (adaptations) occur to the
heart and peripheral vascular system in
response to the haemodynamic changes
associated with heart failure.
These physiological changes are
compensatory and maintain cardiac
output and peripheral perfusion.
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However, as heart failure progresses,
these mechanisms are overwhelmed
and become pathophsiological.
Most important among these
adaptations are: the (1) Frank-Starling
mechanism, in which an increased
preload helps to sustain cardiac
performance;
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(2) myocardial hypertrophy with or
without cardiac chamber dilatation, in
which the mass of contractile tissue is
augmented .
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(3) activation of neurohumoral systems,
especially the release of norepinephrine
(NE) by adrenergic cardiac nerves,
which augments myocardial contractility
and the activation of the reninangiotensin-aldosterone system (RAAS)
and other neurohumoral adjustments
that act to maintain arterial pressure
and perfusion of vital organs.
Types of heart failure:
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Left versus right HF
Systolic versus diastolic HF
High-output versus low-output HF
Acute versus chronic HF
Dominant systolic heart failure
Ischemic
myocardial
disease, coronary
artery disease
 Alcoholic
cardiomyopathy
 Diabetic
cardiomyopathy
 Cocaine
cardiomyopathy
 Drug-induced
cardiomyopathy
(eg, doxorubicin)
Idiopathic
cardiomyopathy
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Peripartum
cardiomyopathy
Myocarditis
Preterminal
valvular heart
disease
Congenital heart
disease with
severe pulmonary
hypertension
Terminal
ventricular septal
defect or atrial
septal defect
Dominant diastolic heart
failure
Hypertension
 Severe aortic stenosis
 Hypertrophic cardiomyopathy
 Restrictive cardiomyopathy
 Ischemic myocardial disease,
coronary artery disease
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High-output heart failure
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Anemia
Systemic
arteriovenous
fistulas
Hyperthyroidism
Beriberi heart
disease
Paget disease of
bone
Multiple myeloma
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Pregnancy
Glomerulonephrits
Cor pulmonale
Polycythemia vera
Carcinoid
syndrome
Obesity
Acute heart failure
Acute mitral or aortic regurgitation
 Rupture of valve leaflets or
supporting structures
 Infective endocarditis with acute
valve incompetence
 Myocardial infarction
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DIAGNOSIS
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Clinical presentation:
Clinical manifestations of HF vary depending
on the rapidity of cardiac decompensation,
underlying etiology, age, and comorbidities of
the patient.
Extreme deterioration in cardiac output and
elevated SVR result in hypoperfusion of vital
organs such as the kidney and brain and
ultimately, cardiogenic shock.
Symptoms:
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Fatigue
Exercise intolerance
Dysnea with exertion
Orthopnea,PND
Palpitation
Physical examination
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Chronic pulmonary and systemic venous
congestion results in pulmonary
crackles. Peripheral edema, high JVP,
pleural and pericardial effusions,
hepatic congestion, and ascites.
3rd or 4th heart sounds may be present
Physical examination
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Edema, in the absence of dyspnea or
other signs of LV or RV failure, is not
solely indicative of heart failure and can
be observed in many other conditions,
including chronic venous insufficiency,
nephrotic syndrome, or other
syndromes of hypoproteinemia or
osmotic imbalance .
Physical examination
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Hepatomegaly is prominent in patients with
chronic right-sided heart failure, but it may
occur rapidly in acute heart failure .
When occurring acutely, the liver is usually
tender .
In patients with considerable tricuspid
regurgitation, a prominent systolic pulsation
of the liver, attributable to an enlarged right
atrial V wave, is often noted.
Physical examination
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Pulsus alternans occurs most commonly
in heart failure due to increased
resistance to LV ejection, as occurs in
hypertension, aortic stenosis, coronary
atherosclerosis, and dilated
cardiomyopathy
Physical examination
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Mitral and tricuspid regurgitation
murmurs are often present in patients
with decompensated heart failure
because of ventricular dilatation. These
murmurs often disappear or diminish
when compensation is restored
Physical examination
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Cardiac cachexia is found in longstanding heart failure, particularly of the
RV, because of anorexia from hepatic
and intestinal congestion and
sometimes because of digitalis toxicity.
Occasionally, impaired intestinal
absorption of fat and (rarely) proteinlosing enteropathy occur
Laboratory studies:
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B-typenatriuretic peptide (BNP) is
synthesized by right and left ventricular
myocytes and released in response to
stretch, volume overload, and elevated
filling pressure. Serum levels pf( BNP)
are elevated in patients with
asymptomatic LV dysfunction as well as
symptomatic HF.
Laboratory studies:
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A serum BNP of less than 100pg-ml has
a good –ve predictive value &typically
excludes HF as primary diagnosis in
dyspeic patients.
BNP levels correlate with severity of HF
and predict survival.
Laboratory studies
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Associated laboratory abnormalities
include elevated levels of blood urea
nitrogen and creatinine, hyponatreamia,
anemia, and elevated serum levels of
hepatic enzymes.
Imaging
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Abnormalities in the (ECG) are common and
supra ventricular and ventricular arrhythmias,
conduction delays, and non specific ST-T
changes.
Radiographic evidence of cardiomegaly and
pulmonary vascular redistribution in common.
Depressed ventricular function should be
confirmed by echocardiography .radionuclide
ventricuography, or cardiac catheterization
with left ventriculography.
Staging
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A classification of patients with heart
disease based on the relation between
symptoms and the amount of effort
required to provoke them has been
developed by the NYHA .
Staging
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Class I: No limitations
Class II: Slight limitation of physical
activity
Class III: Marked limitation of physical
activity
Class IV: Symptomatic at rest.
Symptoms of CHF are present at rest.
Treatment and mangement:
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Medical therapy of heart failure focuses
on 3 main goals: (1) preload reduction,
(2) reduction of systemic vascular
resistance (afterload reduction), and (3)
inhibition of both the RAAS systems and
vasoconstrictor neurohumoral factors
produced by the sympathetic nervous
system in patients with heart failure
Aims of heart failure
management ;
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To achieve
improvement in
symptoms :
Diuretics
Digoxin
ACE inhibitors
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To achieve
improvement in
survival:
ACE inhibitors
ß blockers (for
example, carvedilol
and bisoprolol)
Oral nitrates plus
hydralazine
Drugs:
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1-Diuretics; loop diuretics routinely used to
relieve symptoms e.g. furosemide 40 mg -24h
PO; increase the dose as necessary .SE:
hypokaleamia, renal impairment. Monitor
U &E and add K+ sparing diuretic if K IS less
than 3.2mmol-L,concurrent digoxin therapy (
decreased k+ increase risk of digoxin
toxicity),or pre-existing k+-loosing conditions.
If refractory edema, consider adding a
thiazide e.g. metolazone 5-20mg per 24h PO.
Drugs:
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2-ACE-inhbitor: consider in all patient
with ventricular systolic dysfunctions. It
improves symptoms and prolongs life. If
cough is a problem an ARBs may be
substituted.
Drugs:
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3-B-blockers: eg carvedilol, recent
randomized trials show that B-blocker
decrease mortality in heart failure.
Should be initiated after diuretic
andACE-i.use with caution; start low
and go slow.
Drugs:
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4- Spironolactone: the rales trial
showed that spironolactone (25mg-24h
PO) decrease mortality by 30%when
added to conventional therapy. It
should be initiated in patients who
remain symptomatic despite optimal
therapy as listed above.
Drugs:
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5- digoxin: improves symptoms even in
those with sinus rhythm .use it if
diuretics, ACE –I and B- blocker do not
control symptoms or in patient AF.dose;
0.0125-0.25mg-24h PO. Monitor U&E,
maintain k + at 4-5 mmol-L.
Drugs:
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6- Vasodilators; the combination of
hydralazine (SE; drug induced lupus)
and isosorbide dinitrate should be used
in combination in people intolerant of
an ACE-I or ARBs as it reduces
mortality.
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Hydralazine has one main advantage
over ACE inhibitors in that it is safe in
pregnancy. It also is not known to
worsen renal function in patients with
heart failure who have reduced renal
function and is not associated with the
risk of hyperkalemia .
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Diet:
Patients admitted with heart failure or
pulmonary edema should maintain a
low-salt diet in order to minimize fluid
overload. Monitor fluid balance closely
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Activity:
Patients with decompensated heart failure
should be placed on complete bed rest until
their decompensation is resolved. This is
necessary to maximally reduce myocardial
oxygen demand and to avoid exacerbation of
the abnormal hemodynamics and symptoms
of heart failure
Surgery
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Ventricular assist devices:intractable
cardiogenic shock after acute MI,and
for patients who get worse while
waiting for tranplantation.
Cardiac transplantation
Thank you