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There will an increase in vascular compression in chronic liver disease.

When the
liver is damaged, stellate cells are activated and transformed into myofibroblasts which
contract under the influence of mediators such as endothelin and prostaglandins. Due to
this, sinusoidal space will reduce in diameter which result increase resistance of blood
to flow to the liver and decreased blood flow to the liver. This will then lead to portal
congestion. To maintain a constant inflow of blood to the liver, hepatic artery blood flow
is inversely related to portal vein flow. So there will be increase flow through the hepatic
artery and then increase blood volume in sinusoid and vein. This will then lead to
congestion. Obstruction of blood ow and development of portal hypertension produces
an increase in the hydrostatic pressure within the peritoneal capillaries which results to
ascites. Ascites is also a result of a decrease in oncotic pressure (which causes fluid to
remain within the blood stream instead of leaking out into the tissues) due to a low
albumin level which allows fluid to leak out from the interstitial spaces into the peritoneal
cavity.
Portal Hypertension also leads to the development of new veins also called as
collateral veins. Portosystemic collaterals shunt blood away from the liver. Hence, less
blood reaches the liver when portal flow increases. Due to this bypass, toxins are not
normally shunted to the systemic circulation. In the case of Patient XY, collateral vessels
developed at the lower end of the esophagus and at the upper part of the stomach. The
vessels then became enlarged and full of twists and turns. These vessels became
varicose veins in the esophagus, also known as esophageal varices. The
extra blood flow causes the veins in the esophagus to balloon outward. Prior to
admission, Patient XYs esophageal varices ruptured and massive bleeding in the upper

gastrointestinal tract then occurred. Patient XY manifested melena, hematemesis and


lightheadedness, which are some of the signs and symptoms of ruptured esophageal
varices.
Due to the massive blood loss, hypovolemic shock begins with a decrease in the
intravascular volume. This results in decreased venous return of blood to the heart and
subsequent decreased ventricular lling. Decreased ventricular lling results in
decreased stroke volume (amount of blood ejected from the heart) and decreased
cardiac output. When cardiac output drops, blood pressure drops and tissues cannot be
adequately perfused. The compensatory mechanism of the body will then occur. Atrial
volume receptors sense the drop of the blood volume and stimulate the release of the
antidiuretic hormone (ADH) from the pituitary gland, which reduces water excretion
through the kidneys. Decreased perfusion of the juxtaglomerular apparatus in the
kidneys stimulates renin-angiotensin system and finally aldosterone release from the
adrenal cortex, which causes the retention of sodium and hence water in the kidneys,
which helps to maintain blood volume. Baroreceptors detects decrease in blood
pressure, which then activate the sympathetic systemsympathetic nerves, which
release

norepinephrine

(noradrenaline)

and

adrenal

medulla,

which

releases

epinephrine, which results in the constriction of the peripheral blood vessels in the skin
and increased heart contractility and heart rate. Hypovolemic shock also occurs when
there is a reduction in intravascular volume of 15% to 25%. Intravascular volume can be
reduced both by uid loss and uid shifting between the intravascular and interstitial
compartments. This three process leads to increase cardiac ouput. However, when the
cause of crisis is not resolved, compensatory mechanisms eventually become

overwhelmed and there will be continuous volume loss, decrease in cardiac output and
tissues cannot be adequately perfused. Eventually, cellular metabolism is unable to
generate enough energy to maintain cellular homeostasis. This leads to impairment of
the cell membrane ion pump, accumulation of intracellular sodium and the loss of
intracellular potassium. The cell swells, ruptures and dies. When the shock is not
resolved, multiple organ failure will then happen.