CHF (Handout, B. Shah, 2005)

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CONGESTIVE HEART FAILURE
Brijen J. Shah, MD
July 17, 2005
Goals:
1.
2.
3.
4.
5.
To review the etiology and basic pathophysiology concepts related to congestive heart failure.
To understand the difference between right and left sided heart failure
To identify symptoms from the history and physical exam findings related to CHF
To be able to generate the elements needed for an initial workup of CHF
To outline strategies of CHF therapy as it relates to mechanism of disease
A. Pathophysiology
Two main entities which determine the mechanism of disease: systolic dysfunction and diastolic
dysfunction.
1. Systolic dysfunction, relating to the pumping mechanism of the heart.
-Decreased contractility
Etiologies: MI(62%), valvular heart disease, HTN (10%), cardiomyopathy
Arch Intern Med 2001 Apr 9;161(7):996-1002.
-Increased afterload related to HTN
-Body’s own compensation: In CHF, the heart undergoes certain changes which allow it to maintain it’s
equilibrium. It’s when these mechanisms are maximized that a CHF exacerbation may occur.
a. Frank-Straling curve represents the mechanical relationship between muscle fibers and volume. With
regards to CHF, increased volume (end-diastolic volume due to poor systolic emptying) leads to increased
stretch of myofibers/cross links which then increase contractility.
b. Hypetrophy.
-Increased inotropy by endogenous catecholamines.
2. Diastolic dysfunction relating to active relaxation in early diastole and passive filling.
B. Right vs left heart failure
Left heart failure is related to any process that effects the left side such as an left ventricular ischemic
event.
Right sided hear failure which is most commonly due to left sided heart failure and COPD.
C. Symptoms
These can be divided into symptoms of excess fluid accumulation and symptoms related to decreased
cardiac output. The chronicity of these symptoms can help determine the underlying cause.
Dyspnea (from vascular congestion and decreased CO), orthopnea, PND, edema (related to disequilibrium
in Starling Forces), anorexia, fatigue, bowel distention, palpitations, lightheadnedd
New York Heart Association classification of heart failure is based on symptoms and activity level. Class I
(few symptoms at high levels of activity) to class IV (symptoms at rest).
D. Physical Exam
The multiple mechanisms resulting in CHF also determine the physical findings.
Mechanism
Decreased cardiac output
Volume overload
Ventricular enlargement
Pulmonary HTN
Physical Exam
Sinus tachycardia, diaphoresis; cool, pale and cynatoic limbs,
palpable dichotic notch, pulsus alternans
Rales peripheral edema- ascites, hepatomegaly, splenomegaly
elevated JVP
S3, laterally displaced PMI
Accentuated P2
E. Diagnostic Tests
Blood test- CBC can reveal an anemia which could exacerbate CHF. Chemistries are important in
determining treatment and baseline renal function (creatinine, potassium). LFTs can be elevated with
hepatic congestion. Thyroid function as hypothyroidism and thyrotoxicosis can present as heat failure. BNP
is a substance released in response to high ventricular filling and elevated values have been shown to
coorelate with CHF. N Engl J Med 2002 Jul 18;347(3):161-7.
ECG- Although any new finding for a patient with new CHF could lead the underlying cause, in most
patients it is important to look for evidence of ischemia (ST segment changes, T wave inversions) or atrial
fibrillation. Assess voltage for left ventricular hypertrophy.
CXR- cardiomegaly, Kerley B lines, pulmonary effusion, vascular congestion
ECHO- This 2D test can help to assess for valvular abnormalities, right ventricular size, left systolic
function.
Cardiac catheterization- Helpful in looking for chamber pressures, pulmonary artery hypertension,
shunts, as well as flow limiting lesions for ischemia.
F. Treatment
Correct underlying cause, ie. valvular disease!
Mechanism/Symptom
Systolic Dysfunction
Contractility
Reducing afterload
Reducing preload and LV
pressure
Increased catecholamines
Pulmonary edema
Diastolic heart failure
Agents
Digoxin, beta agonists
(dobutamine), PDE inhibitors
(milrinone, amrinone)
ACEI, nitrates, hydralizine
Diuretics and vasodilators
Beta blocker
Oxygen, furosemide, morphine,
nitroprusside, intubation
Diuretics, beta blocker
Long term: cardiac rehabilitation, cardiac transplantation
Additional Bibliography:
Harrison’s Principles of Internal Medicine, 15th edition.
Lilly L. et al, Pathophysiology of Heart Disease. “Congestive Heart Failure”
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