Download HEART FAILURE

‫‪HEART FAILURE‬‬
‫غفران أجياد ثامر‬
‫فرح عماد‬
HEART FAILURE
A state that develops when the heart fails
to maintain an adequate cardiac output to
meet the demands of the body
characterized by:
1. Diminished cardiac output (forward
failure)
2. Damming back of blood in the venous
system (backward failure) or Both .
TYPES OF HEART FAILURE
*Left sided ,right sided & biventricular heart
failure
*Acute &chronic heart failure
*Compensated & decompensated heart
failure
* Forward & backward heart failure
* Systolic & diastolic dysfunction
Pathophysioylogy of H.F
Before reaching H.F we have many
mechanisms that is compensatory
mechanisms :
Adaptive mechanisms
by which the CVS maintains arterial pressure &
perfusion of vital organs :
The Frank-Starling mechanism : >preload of .1
dilation helps to sustain cardiac performance by
enhancing contractility.
Myocardial structural change : Augmented .2
muscle mass (hypertrophy) with or without
cardiac chamber dilatation.
Activation of neurohumoral system : .3
Release of norepinephrine – >heart rate—
augments myocardial contractility.
Activation of renin – angiotensin – aldosterone
system.
Release of atrial natriuretic peptide.
Pathophysiology
Failure of adaptive mechanisms
Heart
failure
Pathophysiology
Systolic dysfunction:
Progressive detoriation of
myocardial contractile
function.
Occurs in cases of
Ischemic injury, pressure
or volume overload and
DCM.
E.g. IHD and HTN.
Diastolic dysfunction:
Inability of the heart
chamber to relax, expand,
and fill sufficiently during
diastole to accommodate
an adequate ventricular
blood volume.
E.g. Massive LVH,
myocardial fibrosis,
deposition of amyloid, or
constrictive pericarditis.
Pathophysiology
The onset of HF is preceded by Cardiac
hypertrophy : compensatory response of
the myocardium to > mechanical work.
The stimuli > the rate of protein synthesis,
the amount of protein in each cell, size of
myocytes, numbers of sacromeres &
mitochondria :
the mass & size of heart.
Also accompanied by selective up regulation
of several immediate early response
gene & embryonic forms of contractile
& other proteins.
Schematic representation of the sequence of events in cardiac hypertrophy and its
progression to heart failure, emphasizing cellular and extracellular changes
LEFT SIDED HEART FAILURE
Progressive damming of the blood within the
pulmonary circulation and the consequence
of diminished peripheral BP and flow.
CAUSES :
* IHD
* SYSTEMIC HTN
* MI
* VALVULAR DISEASE
* Non_ischemic myocardial disease
MORPHOLOGY OF LEFT SIDED
HEART FAILURE
HEART:
LEFT VENTRICLE is usually hypertrophied
and often dilated
Secondary enlargement of the left atrium
LUNG:
Pressure in the pulmonary veins are
transmitted retrograde to the capillaries and
arteries
Pulmonary congestion & edema
Heavy wet lung
Kidney:
Decrease cardiac output
Reduction in renal perfusion
Activation of renal – angiotensin –aldosterone
System
Retention of salt & water with consequent
expansion of the interstitial fluid and blood
volumes
Pulmonary edema in lungs
Brain:
Hypoxic encephalopathy
Congestion & edema
Pulmonary congestion with dilated capillaries and leakage of blood into alveolar
spaces leads to an increase in hemosiderin-laden macrophages,
as seen here.
RIGHT SIDED HEART FAILURE
* Usually as a consequence of right sided
heart failure
* Cor pulmonale :chronic severe
pulmonary hypertension due to
increased resistance within the
pulmonary circulation.
* Other causes : multiple pulmonary emboli
& valvular disease
MORPHOLOGY OF RIGHT SIDED
HERTE FAILURE
HEART:
Hypertrophy and dilation are generally
confined to right ventricle and atrium.
LIVER AND PORTAL SYSTEM:
* Passive congestive hepatomegaly(nutmeg
liver)
* Centrilobular necrosis along with the
sinusoidal congestion
* Congestive splenomegaly
* Ascites
Here is an example of a "nutmeg" liver seen with chronic passive congestion of the liver.
Note the dark red congested regions that represent accumulation
of RBC's in centrilobular regions. the natural nutmeg is at right.