A bruise, also known as a contusion, is a type of hematoma of tissue, the most common cause being capillaries damaged by trauma, causing localized bleeding that extravasates into the surrounding interstitial tissues. Most bruises are not very deep under the skin so that the bleeding causes a visible discoloration. The bruise then remains visible until the blood is either absorbed by tissues or cleared by immune system action. Bruises which do not blanch under pressure can involve capillaries at the level of skin, subcutaneous tissue, muscle, or bone. Bruises are not to be confused with other similar-looking lesions. (Such lesions include petechia (less than 3 mm (0.12 in), resulting from numerous and diverse etiologies such as adverse reactions from medications such as warfarin, straining, asphyxiation, platelet disorders and diseases such as cytomegalovirus), purpura (3–10 mm (0.12–0.39 in), classified as palpable purpura or non-palpable purpura and indicates various pathologic conditions such as thrombocytopenia),  and ecchymosis (more than 1 cm (0.39 in), caused by blood dissecting through tissue planes and settled in an area remote from the site of trauma or pathology such as periorbital ecchymosis, e.g. "raccoon eyes", arising from a basilar skull fracture or from a neuroblastoma).As a type of hematoma, a bruise is always caused by internal bleeding into the interstitial tissues which does not break through the skin, usually initiated by blunt trauma, which causes damage through physical compression and deceleration forces. Trauma sufficient to cause bruising can occur from a wide variety of situations including accidents, falls, and surgeries.
Pathophysiology
The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape. This process is usually associated with a continuous decline in ejection fraction. The concept of cardiac remodeling was initially developed to describe changes that occur in the days and months following myocardial infarction. Compensation effects
As DCM progresses, two compensatory mechanisms are activated in response to impaired myocyte contractility and reduced stroke volume:
Frank-Starling law
Neurohormonal feedback, via activation of the sympathetic nervous system and the renin-angiotensin system.These responses initially compensate for decreased cardiac output and maintain those with DCM as asymptomatic. Eventually, however, these mechanisms become detrimental, intravascular volume becomes too great, and progressive dilatation leads to heart failure symptoms. Computational models
Cardiac dilatation is a transversely isotropic, irreversible process resulting from excess strains on the myocardium. A computation model of volumetric, isotropic, and cardiac wall growth predicts the relationship between cardiac strains (e.g.