Heart Failure-bds 2012
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Transcript of Heart Failure-bds 2012
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Heart FailureDr. Ibrahim Y Hachim
The FrankStarling law
states that the greater the
volume of blood entering the
heart during diastole (end-
diastolic volume), the greater
the volume of blood ejected
during systolic contraction
(stroke volume) and vice-
versa.
http://upload.wikimedia.org/wikipedia/commons/0/01/Starling_RAP_combined.svg -
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What is Heart Failure? I t i s a pathologic state in which impaired
cardiac function renders the heart unable to
maintain output sufficient for the metabolic
requirements of the body.
Common end point of many forms of heart
disease .
Heart Failure CHF is ccc by diminished cardiac output
(forward failure) , accumulation of blood in thevenous system ( backward failure) , or both.
cardiac output( forward failure)
accumulation ofblood in the venoussystem ( backwardfailure)
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Most instances of heart failure
are the consequences of
progressive detorioration of
myocardial contractilefunction (systolic
dysfunction).
Frequently due to ischemic
injury , pressure or volume
overload , or dilated
cardiomyopathy .
Occasionally , failure results
from inability of the heart
chambers to relax
sufficiently during diastole
(diastolic dysfunction) .
This can occur with massive
left ventricular
hypertrophy , deposition ofamyloid , or constrictive
pericarditis.
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Inadequate cardiac output in CHF
Tachycardia Blood volumeexpansion bysalt and waterretension.
Ventricular dilation ( improves contraction by myofiber stretchingaccording to the Frank-Starling law).
LEFT-SIDED HEART FAILURE
ischemic heart disease hypertension aortic and mitralvalvular diseases
nonischemicmyocardialdiseases
Involves the left ventricle (lower chamber) of theheart
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Morphology.The findings in the heart vary depending on the cause of the
disease process; abnormalities such as myocardial infarction or
a valvular deformity may be present. This chamber is usually
hypertrophied and often dilated, sometimes quite
massively except with obstruction at the mitral valve or other
processes that restrict the size of the left ventricle,
Secondary enlargement of the left atrium with resultant atrial
fibrillation (i.e., uncoordinated contraction of the atrium) may
either compromise stroke volume or cause blood stasis and
possible thrombus formation. A fibrillating left atrium carries a
substantially increased risk of embolic stroke..
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LungsPressure in the pulmonary veins mounts and is ultimately
transmitted retrograde to the capillaries and arteries. The result
is pulmonary congestion and edema, with heavy, wet lungs.
LungsIt is sufficient to note here that the pulmonary changes include,in sequence:-(1) a perivascular and interstitial transudate, particularly in theinterlobular septa, responsible for Kerley's B lines on x-ray
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(2) Progressive edematous widening of alveolar septa
(3) Accumulation of edema fluid in the alveolar spaces.
Moreover, hemosiderin-containing macrophages in the alveoli
(called siderophages, or heart failure cells) denote previous
episodes of pulmonary edema.
Dyspnea (breathlessness), usually the earliest and thecardinal complaint of patients in left-sided heart failure.With further impairment, there is orthopnea, which isdyspnea on lying down that is relieved by sitting orstanding. Thus the orthopneic patient must sleep whilesitting upright. Paroxysmal nocturnal dyspnea is anextension of orthopnea. Cough is a commonaccompaniment of left-sided failure.
Clinical manifestations
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Decreased cardiac outputKidneys
reduction in renal perfusion
The renin-angiotensin-aldosterone
THE RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
ACE
ACE INHIBITORS
JGA
RENIN
ADRENAL
ALDOSTERONE
ANGIOTENSINOGEN ANGIOTENSIN 1
ANGIOTENSIN 2
VASOCONSTRTICTS
Na RETENTION
INCREASED BP
If the perfusion deficit of thekidney becomes sufficientlysevere, impaired excretionof nitrogenous productsmay cause azotemia, in thisinstance prerenal azotemia
Poor renal perfusion is sensed by the
juxtaglomerular apparatus, which secretesrenin. Renin converts angiotensinogen inthe blood to angiotensin1. This in turn isconverted by ACE (angiotensin convertingenzyme) to angiotensin2, which increasesblood pressure directly by vasoconstrictionand by increasing adrenal secretion ofaldosterone. ACE inhibitors are used totreat heart failure as well. as hypertension.Diuretic drugs are another mainstay oftreatment.
BrainIn far-advanced CHF, cerebral hypoxia may give rise tohypoxic encephalopathy , with irritability, loss ofattention span, and restlessness, which may evenprogress to coma.
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What is Right Heart Failure?
Isolated right-sided heart failure occurs in only a few
diseases. Usually it is a secondary consequence of left-
sided heart failure because any increase in pressure inthe pulmonary circulation incidental to left-sided heart
failure inevitably produces an increased burden on the
right side of the heart.
Cor pulmonale is the term given to heart failure due tolung disease, such as chronic obstructive airwaysdisease.
The major morphologic and clinical effects of pure right-
sided heart failure differ from those of left-sided heart
failure in that pulmonary congestion is minimal,
whereas engorgement of the systemic and portal venous
systems may be pronounced.
Right-sided HF
Liver and Portal System
Kidneys
BrainPleural and Pericardial Spaces
SubcutaneousTissues
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1
The liver is usually increased in size and weight (congestivehepatomegaly), and a cut section displays prominent
passive congestion . Congested red centers of the liverlobules are surrounded by paler, sometimes fatty, peripheralregions (nutmeg liver).
The liver
Centralvein
Right-sided heart failure also leads to elevated pressure inthe portal vein and its tributaries. Congestion produces atense, enlarged spleen (congestive splenomegaly).
Kidneys
Congestion of the kidneys is more marked with right-
sided heart failure than with left-sided heart failure,
leading to greater fluid retention, peripheral edema,
and more pronounced azotemia.
Brain
Symptoms essentially identical to those described inleft-sided heart failure may occur, representing venous
congestion and hypoxia of the central nervous system.
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Subcutaneous Tissues
Peripheral edema of dependent portions of the
body, especially ankle (pedal)
and pretibial edema, is a
hallmark of right-sided heart
failure. In chronically
bedridden patients, the
edema may be primarily
presacral. Generalizedmassive edema is called
anasarca.