Transcript Congestive Heart Failure: From Basics to Recent Advances

By:Dawit Ayele(MD,Internist)
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“Heart (or cardiac) failure is the pathophysiological state in which
the heart is unable to pump blood at a rate commensurate with
the requirements of the metabolizing tissues or can do so only
from an elevated filling pressure.”
- Eugene Braunwald
“Congestive heart failure (CHF) represents a complex clinical
syndrome characterized by abnormalities of left ventricular
function and neurohormonal regulation, which are accompanied
by effort intolerance, fluid retention, and reduced longevity”
- Milton Packer
􀁺 Burden of CHF is staggering
􀁺 5 million in US (1.5% of all
adults)
􀁺 500,000 cases annually
􀁺 In the elderly
􀁺 6-10% prevalence
􀁺 80% hospitalized with HF
􀁺 250,000 death/year
attributable to CHF
􀁺 $38 billion (5.4% of
healthcare cost)
◦ Coronary artery
disease◦ HTN--both
◦ Valvular heart
disease (especially
aorta and mitral
disease)--chronic
◦ Congenital
◦ Alcohol-◦ Diabetes—
◦ Cardiomyopathies
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Infection
Arrhythmia
Physical,Fluid,Dietary,Env’tal,Emotional excess
MI
Anemia
Pulmonary embolism
Worsening of HTN
Thyrotoxicosis
Infective endocarditis
Rheumatic,viral or other myocarditis..
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SYSTOLIC VERSUS DIASTOLIC FAILURE
LOW-OUTPUT VERSUS HIGH-OUTPUT HEART
FAILURE
ACUTE VERSUS CHRONIC HEART FAILURE
RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE
BACKWARD VERSUS FORWARD HEART
FAILURE
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1. Syndrome of decrease exercise tolerance
2. Syndrome of fluid retention
3. No symptoms but incidental discovery of
LV
dysfunction
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Major Criteria
􀁺 Orthopnea/PND
􀁺 Venous distension
􀁺 Rales
􀁺 Cardiomegaly
􀁺 Acute pulm edema
􀁺 Elevated JVP
􀁺 HJR
􀁺 Circ time >25s
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􀁺 Minor Criteria
􀁺 Ankle edema
􀁺 Night cough
􀁺 Exertional dyspnea
􀁺 Hepatomegaly
􀁺 Pleural effusion
􀁺 Tachycardia (>120)
􀁺 Decrease VC
􀁺 Weight loss with CHF
tx
Framingham Criteria
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Class I: Symptoms with more than ordinary
activity
Class II: Symptoms with ordinary activity
Class III: Symptoms with minimal activity
Class IIIa: No dyspnea at rest
Class IIIb: Recent dyspnea at rest
Class IV: Symptoms at rest
At Risk for Heart Failure:
STAGE A High risk for developing HF
STAGE B
Asymptomatic LV dysfunction
Heart Failure:
STAGE C Past or current symptoms of HF
STAGE D End-stage HF
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Designed to emphasize preventability of HF
Designed to recognize the progressive
nature of LV dysfunction
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COMPLEMENT, DO NOT REPLACE NYHA CLASSES
NYHA Classes - shift back/forth in individual
patient (in response to Rx and/or
progression of disease)
Stages - progress in one direction due to
cardiac remodeling
◦ Occurs when the left
ventricle fails as an
effective forward pump
◦ back pressure of blood
into the pulmonary
circulation
◦  pulmonary edema
◦ Cannot eject all of the
blood delivered from the
right heart.
◦ Left atrial pressure rises
 increased pressure in
the pulmonary veins and
capillaries
◦ When pressure
becomes too high,
the fluid portion of
the blood is forced
into the alveoli.
◦ decreased
oxygenation capacity
of the lungs
◦ AMI common with
LVF, suspect
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Severe resp.
distress–
◦ Diaphoresis—
 Evidenced by
orthopnea, dyspnea
 Hx of paroxysmal
nocturnal dyspnea.
◦ Pulmonary
congestion
◦ Severe apprehension,
agitation,
confusion—
 Resulting from hypoxia
 Feels like he/she is
smothering
◦ Cyanosis—
 Results from
sympathetic stimulation
 Often present
 Rales—especially at the
bases.
 Rhonchi—associated
with fluid in the larger
airways indicative of
severe failure
 Wheezes—response to
airway spasm
◦ Jugular Venous Distention—
not directly related to LVF.
 Comes from back pressure
building from right heart
into venous circulation
◦ Vital Signs—
 Significant increase in
sympathetic discharge to
compensate.
 BP—elevated
 Pulse rate—elevated to
compensate for decreased
stroke volume.
 Respirations—rapid and
labored
◦ Neurohormonal system
◦ Renin-angiotensin-aldosterone system
◦ Ventricular hypertrophy
Myocardial Disease
Impedance
Vasoconstriction
LV Dysfunction
Neurohormonal
Activation
Renal Blood Flow
Preload
Na Retention
LV Remodeling
Vascular
Remodeling
◦ Decreased renal blood flow secondary to
low cardiac output triggers renin secretion
by the kidneys
 Aldosterone is released  increase in
Na+ retention  water retention
 Preload increases
 Worsening failure
◦ Long term compensatory mechanism
◦ Increases in size due to increase in work
load ie skeletal muscle
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Principles:thorough Hx & P/E
 Supplemental investigations
especially:BNP,ECG,Echocardiography,CXR
Management:(1) general measures;
(2) correction of the underlying cause;
(3) removal of the precipitating cause;
(4) prevention of deterioration of
cardiac function; and
(5) control of the congestive HF state
Control Volume
Diuretic
Slow Disease Progression
RAAS
Inhibition
+
Beta-Blockade
Treat residual
symptoms
SPIRONOLACTONE
DIGOXIN
Am J Cardiol 1999;83(suppl 2A):9A-38A